What is a novel coronavirus?

A novel coronavirus is a new coronavirus that has not been previously identified. The virus causing coronavirus disease 2019 (COVID-19), is not the same as the coronaviruses that commonly circulate among humans and cause mild illness, like the common cold.

A diagnosis with coronavirus 229E, NL63, OC43, or HKU1 is not the same as a COVID-19 diagnosis. Patients with COVID-19 will be evaluated and cared for differently than patients with common coronavirus diagnosis.

Severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2) is the virus that causes COVID-19 (coronavirus disease 2019), the respiratory illness responsible for the COVID-19 pandemic. Also colloquially known simply as the coronavirus, it was previously referred to by its provisional name, 2019 novel coronavirus (2019-nCoV), and has also been called human coronavirus 2019 (HCoV-19 or hCoV-19). The World Health Organization declared the outbreak a Public Health Emergency of International Concern on 30 January 2020, and a pandemic on 11 March 2020. SARS‑CoV‑2 is a positive-sense single-stranded RNA virus that is contagious in humans. As described by the US National Institutes of Health, it is the successor to SARS-CoV-1, the virus that caused the 2002–2004 SARS outbreak.

This timeline provides information about select moments in the COVID-19 pandemic in the United States and around the world beginning from its known origins to today.

[...]

Most adults showed preexisting antibody reactivity against SARS-CoV-2, 90% uninfected adults showed antibody reactivity against spike protein, receptor-binding domain, Nucleocapsid, N-terminal domain

‘Preexisting cross-reactivity to SARS-CoV-2 occurs in the absence of prior viral exposure. However, this has been difficult to quantify at the population level due to a lack of reliably defined seroreactivity thresholds. Using an orthogonal antibody testing approach, we estimated that about 0.6% of nontriaged adults from the greater Vancouver, Canada, area between May 17 and June 19, 2020, showed clear evidence of a prior SARS-CoV-2 infection, after adjusting for false-positive and false-negative test results.

Using a highly sensitive multiplex assay and positive/negative thresholds established in infants in whom maternal antibodies have waned, we determined that more than 90% of uninfected adults showed antibody reactivity against the spike protein, receptor-binding domain (RBD), N-terminal domain (NTD), or the nucleocapsid (N) protein from SARS-CoV-2.

This seroreactivity was evenly distributed across age and sex, correlated with circulating coronaviruses’ reactivity, and was partially outcompeted by soluble circulating coronaviruses’ spike. Using a custom SARS-CoV-2 peptide mapping array, we found that this antibody reactivity broadly mapped to spike and to conserved nonstructural viral proteins. We conclude that most adults display preexisting antibody cross-reactivity against SARS-CoV-2, which further supports investigation of how this may impact the clinical severity of COVID-19 or SARS-CoV-2 vaccine responses.’

At a time when everyone needs better information, from disease modelers and governments to people quarantined or just social distancing, we lack reliable evidence on how many people have been infected with SARS-CoV-2 or who continue to become infected. Better information is needed to guide decisions and actions of monumental significance and to monitor their impact.

Draconian countermeasures have been adopted in many countries. If the pandemic dissipates — either on its own or because of these measures — short-term extreme social distancing and lockdowns may be bearable. How long, though, should measures like these be continued if the pandemic churns across the globe unabated? How can policymakers tell if they are doing more good than harm?

On The Revelations of Pandemic Data

The following interview with Norman Fenton by David Marks presents a comprehensive overview of how pandemic data was skewed to serve the interests of Big Pharma and Government agendas. It is from a new website just launched by Children’s Health Defense, called the Community Forum. In addition to this piece, the Forum will have a number of informative articles and information about advocating and organizing for change.

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Fenton: A good example of how we used Bayesian analysis was to answer the question: Do I, or do I not, have the SARS-CoV-2 (COVID) virus? And specifically, if I'm asymptomatic, what is the probability that I might have the virus? Answering this question correctly was the focus of one of our first inquiries.

Suppose that at a given time there is data available suggesting that, in the general population, one in a thousand asymptomatic people were likely to have the virus. Such data was never confirmed of course, the infection rate varied over time, but I will use it to explain the Bayesian reasoning.

If I take a PCR test and it’s positive but I’m not feeling ill, I would want to know if I really have the virus. In other words, if I am one — of the one-in-a-thousand people — who is asymptomatic but carrying the virus, I’d want to know the accuracy of the test. There weren’t any reliable studies about the reliability of the PCR test, but the public was assured these tests were very accurate. Let’s suppose there was only a one-in-a-hundred chance that someone who doesn't have the virus will test positive — a 1% false positive rate. Then conversely, if I don't have the virus, there's a 99% chance of a negative test. With this information most people assumed if you tested positive you almost certainly had COVID. But that is not the case. 

Think about a group of 10,000 asymptomatic people getting tested. Because we are assuming one-in-a-thousand asymptomatic people have the virus, that means about 10 of the 10,000 really have the virus. Let’s also assume these genuinely infected people test positive. Then we are left with just under 10,000 people — 9990, who do not have the virus. But a PCR test with only a 1%false positive rate still means that about 100 of these people would falsely test positive. So in total there are 110 people testing positive of whom we know only 10 will actually become ill from the virus. So, the actual probability that you've got the virus if you test positive is closer to 10%. This means that with reasonable assumptions about the underlying infection rate and test accuracy, the PCR test used as a standard for life-impacting decisions and mandates, had a 99% inaccuracy rate for asymptomatic people testing positive.

The confusion lies with the incorrect assumption that even if you don’t have symptoms of the virus, that the possibility of a false positive in the PCR test is only 1%. As more accurate calculations based on reliable data show, that is clearly not the case. To assume these probabilities are equal is known as the fallacy of the transposed conditional. In the courtroom, when DNA evidence is misinterpreted, it’s called the prosecutor's policy. Those contradictory figures should have raised important questions — it’s not that complicated — it can be presented in a confusing way, but scientists who knew better ignored this data.

Forum: Have the results of that comparative data been confirmed by other studies?

Fenton: We looked at the numbers from a study at Cambridge University where they tested several thousand asymptomatic students for the virus over weeks using pooled PCR testing. And during that period what they found was that very few students tested positive. In fact, over the period, only 43 of the 10,394 tests were positive.

However, unlike what happens in PCR testing in the general population, they did a second confirmatory test on each of the same samples that tested positive. They applied this more reliable, approved standard, where two positives were needed for confirmation; if either one was negative, it meant nobody in the pooled sample was infected. They found 36 out of the 43 samples that had tested positive, when re-tested afterwards, showed negative. So, what they saw was 84% of asymptomatic students showing a positive result on the initial test didn't have the virus, confirming a very high inaccuracy rate.

[...]

ATLANTA, Ga. (WEYI) - The Centers for Disease Control released information showing how many people who died from COVID-19 had comorbidities or underlying conditions as they are sometimes referred to by doctors.

According to the CDC, comorbidity is defined as: " more than one disease or condition is present in the same person at the same time. Conditions described as comorbidities are often chronic or long-term conditions. Other names to describe comorbid conditions are coexisting or co-occurring conditions and sometimes also “multimorbidity” or “multiple chronic conditions."

Comorbidity and underlying conditions can both be used to describe conditions that exist in one person at the same time. These can also contribute to a persons death who has been diagnosed with COVID-19.

The CDC said:

Table 3 shows the types of health conditions and contributing causes mentioned in conjunction with deaths involving coronavirus disease 2019 (COVID-19). For 6% of the deaths, COVID-19 was the only cause mentioned. For deaths with conditions or causes in addition to COVID-19, on average, there were 2.6 additional conditions or causes per death.

The CDC says people need to always social distance and perform best practices when it comes to staying safe during the COVID-19 pandemic.

Key Points

Question What are the characteristics, clinical presentation, and outcomes of patients hospitalized with coronavirus disease 2019 (COVID-19) in the US?

Findings In this case series that included 5700 patients hospitalized with COVID-19 in the New York City area, the most common comorbidities were hypertension, obesity, and diabetes. Among patients who were discharged or died (n = 2634), 14.2% were treated in the intensive care unit, 12.2% received invasive mechanical ventilation, 3.2% were treated with kidney replacement therapy, and 21% died.

Meaning This study provides characteristics and early outcomes of patients hospitalized with COVID-19 in the New York City area.

Abstract

Importance There is limited information describing the presenting characteristics and outcomes of US patients requiring hospitalization for coronavirus disease 2019 (COVID-19).

Objective To describe the clinical characteristics and outcomes of patients with COVID-19 hospitalized in a US health care system.

[...]

Results A total of 5700 patients were included (median age, 63 years [interquartile range {IQR}, 52-75; range, 0-107 years]; 39.7% female). The most common comorbidities were hypertension (3026; 56.6%), obesity (1737; 41.7%), and diabetes (1808; 33.8%). At triage, 30.7% of patients were febrile, 17.3% had a respiratory rate greater than 24 breaths/min, and 27.8% received supplemental oxygen. The rate of respiratory virus co-infection was 2.1%. Outcomes were assessed for 2634 patients who were discharged or had died at the study end point. During hospitalization, 373 patients (14.2%) (median age, 68 years [IQR, 56-78]; 33.5% female) were treated in the intensive care unit care, 320 (12.2%) received invasive mechanical ventilation, 81 (3.2%) were treated with kidney replacement therapy, and 553 (21%) died. As of April 4, 2020, for patients requiring mechanical ventilation (n = 1151, 20.2%), 38 (3.3%) were discharged alive, 282 (24.5%) died, and 831 (72.2%) remained in hospital. The median postdischarge follow-up time was 4.4 days (IQR, 2.2-9.3). A total of 45 patients (2.2%) were readmitted during the study period. The median time to readmission was 3 days (IQR, 1.0-4.5) for readmitted patients. Among the 3066 patients who remained hospitalized at the final study follow-up date (median age, 65 years [IQR, 54-75]), the median follow-up at time of censoring was 4.5 days (IQR, 2.4-8.1).

Conclusions and Relevance This case series provides characteristics and early outcomes of sequentially hospitalized patients with confirmed COVID-19 in the New York City area.

[...]

Objective: To estimate the infection fatality rate of coronavirus disease 2019 (COVID-19) from seroprevalence data.

Methods: I searched PubMed and preprint servers for COVID-19 seroprevalence studies with a sample size ≥ 500 as of 9 September 2020. I also retrieved additional results of national studies from preliminary press releases and reports. I assessed the studies for design features and seroprevalence estimates. I estimated the infection fatality rate for each study by dividing the cumulative number of COVID-19 deaths by the number of people estimated to be infected in each region. I corrected for the number of immunoglobin (Ig) types tested (IgG, IgM, IgA).

Findings: I included 61 studies (74 estimates) and eight preliminary national estimates. Seroprevalence estimates ranged from 0.02% to 53.40%. Infection fatality rates ranged from 0.00% to 1.63%, corrected values from 0.00% to 1.54%. Across 51 locations, the median COVID-19 infection fatality rate was 0.27% (corrected 0.23%): the rate was 0.09% in locations with COVID-19 population mortality rates less than the global average (< 118 deaths/million), 0.20% in locations with 118-500 COVID-19 deaths/million people and 0.57% in locations with > 500 COVID-19 deaths/million people. In people younger than 70 years, infection fatality rates ranged from 0.00% to 0.31% with crude and corrected medians of 0.05%.

Conclusion: The infection fatality rate of COVID-19 can vary substantially across different locations and this may reflect differences in population age structure and case-mix of infected and deceased patients and other factors. The inferred infection fatality rates tended to be much lower than estimates made earlier in the pandemic.

[...]

ABSTRACT

The infection fatality rate (IFR) of COVID-19 among non-elderly people in the absence of vaccination or prior infection is important to estimate accurately, since 94% of the global population is younger than 70 years and 86% is younger than 60 years. In systematic searches in SeroTracker and PubMed (protocol: https://osf.io/xvupr), we identified 40 eligible national seroprevalence studies covering 38 countries with pre-vaccination seroprevalence data. For 29 countries (24 high-income, 5 others), publicly available age-stratified COVID-19 death data and age-stratified seroprevalence information were available and were included in the primary analysis. The IFRs had a median of 0.035% (interquartile range (IQR) 0.013 - 0.056%) for the 0-59 years old population, and 0.095% (IQR 0.036 - 0.125%,) for the 0-69 years old. The median IFR was 0.0003% at 0-19 years, 0.003% at 20-29 years, 0.011% at 30-39 years, 0.035% at 40-49 years, 0.129% at 50-59 years, and 0.501% at 60-69 years. Including data from another 9 countries with imputed age distribution of COVID-19 deaths yielded median IFR of 0.025-0.032% for 0-59 years and 0.063-0.082% for 0-69 years. Meta-regression analyses also suggested global IFR of 0.03% and 0.07%, respectively in these age groups. The current analysis suggests a much lower pre-vaccination IFR in non-elderly populations than previously suggested. Large differences did exist between countries and may reflect differences in comorbidities and other factors. These estimates provide a baseline from which to fathom further IFR declines with the widespread use of vaccination, prior infections, and evolution of new variants.

Highlights *Across 31 systematically identified national seroprevalence studies in the pre-vaccination era, the median infection fatality rate of COVID-19 was estimated to be 0.035% for people aged 0-59 years people and 0.095% for those aged 0-69 years.

*The median IFR was 0.0003% at 0-19 years, 0.003% at 20-29 years, 0.011% at 30-39 years, 0.035% at 40-49 years, 0.129% at 50-59 years, and 0.501% at 60-69 years.

*At a global level, pre-vaccination IFR may have been as low as 0.03% and 0.07% for 0-59 and 0-69 year old people, respectively.

*These IFR estimates in non-elderly populations are lower than previous calculations had suggested.

[...]

To date, we still don’t have especially good studies on the actual causes of excess deaths by state and country when the world first went into lockdown in spring 2020.

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Thus, this article reexamines data from the US CDC on all-cause excess deaths by state during peak lockdown in April 2020 using the information we now know to determine what actually caused them.

This examination concludes that, contrary to popular belief, there was no uniquely deadly strain or variant emanating out of New York in spring 2020; this is clear from the fact that several states close to New York such as Vermont, New Hampshire, and Maine experienced little to no excess deaths during that time period.

On the contrary, over 30,000 Americans appear to have been killed by mechanical ventilators or other forms of medical iatrogenesis throughout April 2020, primarily in the area around New York.

This result is not altogether surprising, as subsequent studies revealed a 97.2% mortality rate among those over age 65 who were put on mechanical ventilators in accordance with the initial guidance from the WHO—as opposed to a 26.6% mortality rate among those over age 65 who weren’t put on mechanical ventilators—before a grassroots campaign put a stop to the practice by the beginning of May 2020.

[...]

PLEASE NOTE: This implementation of the QCovid risk calculator is NOT intended for use supporting or informing clinical decision-making. It is ONLY to be used for academic research, peer review and validation purposes, and it must NOT be used with data or information relating to any individual. For full terms and conditions please see the Academic Licence. For any other use cases, please contact enquiries@innovation.ox.ac.uk quoting reference 17939.

The symptoms of COVID-19 are variable depending on the type of variant contracted, ranging from mild symptoms to critical and possibly fatal illness.^[1][2] Common symptoms include coughing, fever, loss of smell (anosmia) and taste (ageusia), with less common ones including headaches, nasal congestion and runny nose, muscle pain, sore throat, diarrhea, eye irritation,^[3] and toes swelling or turning purple,^[4] and in moderate to severe cases breathing difficulties.^[5] People with the COVID-19 infection may have different symptoms, and their symptoms may change over time. Three common clusters of symptoms have been identified: one respiratory symptom cluster with cough, sputum, shortness of breath, and fever; a musculoskeletal symptom cluster with muscle and joint pain, headache, and fatigue; a cluster of digestive symptoms with abdominal pain, vomiting, and diarrhea.^[5] In people without prior ear, nose, and throat disorders, loss of taste combined with loss of smell is associated with COVID-19 and is reported in as many as 88% of symptomatic cases.^[6][7][8]

Of people who show symptoms, 81% develop only mild to moderate symptoms (up to mild pneumonia), while 14% develop severe symptoms (dyspnea, hypoxia, or more than 50% lung involvement on imaging) which requiring hospitalization and 5% of patients develop critical symptoms (respiratory failure, septic shock, or multiorgan dysfunction) requiring ICU admission.^[9] At least a third of the people who are infected with the virus do not develop noticeable symptoms at any point in time.^[10][11] These asymptomatic carriers tend not to get tested and can still spread the disease.^{[11][12][13][14]} Other infected people will develop symptoms later, called "pre-symptomatic", or have very mild symptoms and can also spread the virus.^[14]

As is common with infections, there is a delay between the moment a person first becomes infected and the appearance of the first symptoms. The median delay for COVID-19 is four to five days^[15] possibly being infectious on 1-4 of those days.^[16] Most symptomatic people experience symptoms within two to seven days after exposure, and almost all will experience at least one symptom within 12 days.^[15][17]

Most people recover from the acute phase of the disease. However, some people – over half of a cohort of home-isolated young adults identified in June, 2021^[18][19] – continued to experience a range of effects, such as fatigue, for months even after recovery. This is the result of a condition called long COVID which can be described as a range of persistent symptoms that continue for weeks and/or months at a time.^[20] Long-term damage to organs has also been observed after the onset of COVID-19. Multi-year studies are underway to further investigate the potential long-term effects of the disease.^[21]

The Omicron variant became dominant in the U.S. starting in December 2021. Symptoms with the Omicron variant are less severe as they are with other variants.^[22]

Managing COVID-19 symptoms

Most people with COVID-19 have mild illness and can recover at home. You can treat symptoms with over-the-counter medicines, such as acetaminophen (Tylenol) or ibuprofen (Motrin, Advil), to help you feel better.

Scientist and Imperial College author Neil Ferguson said Wednesday the coronavirus death toll is unlikely to exceed 20,000 and could be much lower if lockdown measures continue, according to New Scientist. He added that he is “reasonably confident” that Britain’s health system can handle the burden of treating coronavirus patients.

The Infection Fatality Ratio (IFR) estimates the percentage deaths in all those with an infection: the detected (cases) and those with undetected disease (asymptomatic and the not-tested group).

The IFR is used to model the estimated number of deaths in the population at large. If it's a large number approaching one percent, then the modelled outputs can report an alarming number of fatalities - providing the impetus for lockdowns.

Early in the pandemic, Imperial College London’s Report 9 modelled the impact of covid based on a publication by Verity et al. on 13 March 2000, which estimated the IFR as 0.9 percent.

This IFR gave rise to the modelled estimates ‘in an unmitigated epidemic, we would predict approximately 510,000 deaths in GB and 2.2 million in the US.’ 

The authors wrote this: “However, the resulting mitigated epidemic would still likely result in hundreds of thousands of deaths and health systems (most notably intensive care units) being overwhelmed many times over. For countries able to achieve it, this leaves suppression as the preferred policy option.”

A recent publication by Stanford researchers based on seroprevalence studies in the covid pre-vaccination era provides a more robust estimate of the IFR.

Across 32 studies, the median IFR of COVID-19 was estimated to be 0.035% for people aged 0-59 years and 0.095% for those aged 0-69.

We compared the two IFR estimates, which shows the Imperial College estimates are much higher than Stanfords across the age groups.

[...]

The consequences of overestimating the IFR are profound. It overpredicts the number of deaths and influences political decision-making without considering the long-term harm and well-being effects.

Overestimating the IFR is not that unusual. For example, in the Swine flu pandemic, the post-pandemic IFR was reported as 0.02%, fivefold less than the lowest estimate during the outbreak. 

There are further problems with the IFR to consider. First, it assumes all deaths with a PCR positive test or covid on the death certificate were caused by SARs-CoV-2. This Is not the case, as we have shown. The IFR also doesn't account for hospital deaths or the complex interaction of multimorbidity and the assignment of causation.

An analysis distinguishing causation in under 18s, as opposed to those who died of another cause but were coincidentally infected, reported a mortality rate in < 18-year-olds of two per million—suggesting an IFR of 0.0002%, and covid is possibly the underlying cause of death in only about a quarter of young people when it is registered on the death certificate.

Invoking the precautionary principle for the widespread use of restrictions based on catastrophic predictions also underlines the misunderstanding of the basis of the principle: act only when you are sure that the benefits of your actions outweigh the negative consequences. No such evidence existed then, as lockdowns were not even contemplated in the existing pandemic plans.

Background The infection fatality rate (IFR) of Coronavirus Disease 2019 (COVID-19) varies widely according to age and residence status.

Purpose Estimate the IFR of COVID-19 in community-dwelling elderly populations and other age groups from seroprevalence studies. Study protocol: https://osf.io/47cgb.

Data Sources Seroprevalence studies done in 2020 and identified by any of four existing systematic reviews.

[...]

Conclusions The IFR of COVID-19 in community-dwelling elderly people is lower than previously reported. Very low IFRs were confirmed in the youngest populations.

[...]

Abstract

Background: During the current worldwide pandemic, coronavirus disease 2019 (Covid-19) was first diagnosed in Iceland at the end of February. However, data are limited on how SARS-CoV-2, the virus that causes Covid-19, enters and spreads in a population.

[...]

Conclusions: In a population-based study in Iceland, children under 10 years of age and females had a lower incidence of SARS-CoV-2 infection than adolescents or adults and males. The proportion of infected persons identified through population screening did not change substantially during the screening period, which was consistent with a beneficial effect of containment efforts. (Funded by deCODE Genetics-Amgen.).

[...]

Abstract

Background By early April 2020, the COVID-19 pandemic had infected nearly one million people and had spread to nearly all countries worldwide. It is essential to understand where and how SARS-CoV-2 is transmitted.

Methods Case reports were extracted from the local Municipal Health Commissions of 320 prefectural cities (municipalities) in China, not including Hubei province, between 4 January and 11 February 2020. We identified all outbreaks involving three or more cases and reviewed the major characteristics of the enclosed spaces in which the outbreaks were reported and associated indoor environmental issues.

Results Three hundred and eighteen outbreaks with three or more cases were identified, involving 1245 confirmed cases in 120 prefectural cities. We divided the venues in which the outbreaks occurred into six categories: homes, transport, food, entertainment, shopping, and miscellaneous. Among the identified outbreaks, 53·8% involved three cases, 26·4% involved four cases, and only 1·6% involved ten or more cases. Home outbreaks were the dominant category (254 of 318 outbreaks; 79·9%), followed by transport (108; 34·0%; note that many outbreaks involved more than one venue category). Most home outbreaks involved three to five cases. We identified only a single outbreak in an outdoor environment, which involved two cases.

Conclusions All identified outbreaks of three or more cases occurred in an indoor environment, which confirms that sharing indoor space is a major SARS-CoV-2 infection risk.

ABSTRACT

BACKGROUND Since its identification on the 7^th of January 2020, SARS-CoV-2 has spread to more than 180 countries worldwide, causing >11,000 deaths. At present, viral disease and transmission amongst children is incompletely understood. Specifically, there is concern that children could be an important source of SARS-CoV-2 in household transmission clusters.

METHODS We performed an observational study analysing literature published between December 2019 and March 2020 of the clinical features of SARS-CoV-2 in children and descriptions of household transmission clusters of SARS-CoV-2. In these studies the index case of each cluster defined as the individual in the household cluster who first developed symptoms.

FINDINGS Drawing on studies from China, Singapore, South Korea, Japan, and Iran a broad range of clinical symptoms were observed in children. These ranged from asymptomatic to severe disease. Of the 31 household transmission clusters that were identified, 9.7% (3/31) were identified as having a paediatric index case. This is in contrast other zoonotic infections (namely H5N1 influenza virus) where 54% (30/56) of transmission clusters identified children as the index case.

INTERPRETATION Whilst SARS-CoV-2 can cause mild disease in children, the data available to date suggests that children have not played a substantive role in the intra-household transmission of SARS-CoV-2.

[...]

Abstract

Knowledge of the host response to the novel coronavirus SARS-CoV-2 remains limited, hindering the understanding of COVID-19 pathogenesis and the development of therapeutic strategies. During the course of a viral infection, host cells release exosomes and other extracellular vesicles carrying viral and host components that can modulate the immune response. The present study used a shotgun proteomic approach to map the host circulating exosomes' response to SARS-CoV-2 infection. We investigated how SARS-CoV-2 infection modulates exosome content, exosomes' involvement in disease progression, and the potential use of plasma exosomes as biomarkers of disease severity. A proteomic analysis of patient-derived exosomes identified several molecules involved in the immune response, inflammation, and activation of the coagulation and complement pathways, which are the main mechanisms of COVID-19-associated tissue damage and multiple organ dysfunctions. In addition, several potential biomarkers-such as fibrinogen, fibronectin, complement C1r subcomponent and serum amyloid P-component-were shown to have a diagnostic feature presenting an area under the curve (AUC) of almost 1. Proteins correlating with disease severity were also detected. Moreover, for the first time, we identified the presence of SARS-CoV-2 RNA in the exosomal cargo, which suggests that the virus might use the endocytosis route to spread infection. Our findings indicate circulating exosomes' significant contribution to several processes-such as inflammation, coagulation, and immunomodulation-during SARS-CoV-2 infection. The study's data are available via ProteomeXchange with the identifier PXD021144.

Public health officials attempting to contain the new coronavirus are trying to figure out how easily it spreads. One key question is whether people who are infected but show no symptoms can infect other people.

"If you have a lot of people who [have mild disease or are] asymptomatic and not seeking medical care for respiratory illness but are still contagious, you're going to have a very difficult time," says Jeffrey Shaman, a professor of environmental health sciences at Columbia University.

Two previous deadly outbreaks of coronavirus – SARS and MERS – only spread from people who were showing symptoms of disease.

But Shaman has looked at more common coronaviruses, in particular four other coronaviruses that usually don't cause anything more serious than a cold. He's found many people shed those viruses even when they report no symptoms at all. (His results are not peer-reviewed but are available as a preprint).

His study found the coronavirus in the nasal passages of people who didn't report any symptoms, "and it's going to leak out as they're speaking and breathing and coughing and sneezing and wiping their nose," Shaman says. "Whether it's ... a sufficient quantity to make somebody else infectious, we can't discern that from what we've done."

Likewise, it's hard to know what's up with the novel coronavirus. Scientists in Germany reported a case in the New England Journal of Medicine on Jan. 30 in which a visitor from China without symptoms passed the disease along to a colleague in Munich. But, as Science magazine first reported, that was wrong. The woman actually did have symptoms.

[...]

As the coronavirus landed in the U.S. in January, scientists began whispering about an apparent difference from its notorious sibling, the virus that caused SARS: People infected with this one could easily infect others — even if they had no symptoms.

The first reports seemed questionable, and many infectious disease experts didn’t believe them. Two months later, the virus has swarmed across the United States, forcing tens of millions into self-isolation. And now some experts believe that asymptomatic transmission — the passing of a virus from an infected person who feels just fine to others — is driving the pandemic.

Concerns about people without symptoms infecting others were part of the reason county health officers across California, including most of the Bay Area, this week began advising everyone to wear face coverings in public, whether they feel sick or not. The Centers for Disease Control and Prevention issued a nationwide advisory on Friday.

[...]

8 JUN 2020:
Maria Van Kerkhove, head of the World Health Organization’s emerging diseases and zoonosis unit, says transmission of the coronavirus by people who aren’t showing symptoms is "very rare.” She spoke Monday at a briefing in Geneva.

She has just contradicted everything we´ve been hearing for the last four months! She´s destroyed the justification for masks and societal lockdown. Isolation of symptomatic cases (a quarantine) is what should’ve happened from the very beginning. No masks. No social distancing. No lockdowns. Just a good old fashioned quarantine of sick individuals. Not a complete destruction of the world economy causing ripples of closed businesses, unbelievable unemployment, an increasing suicide rate, and general mass fear throughout the world. Shame on these people..This announcement, comes, RIGHT at the moment of the protests and rioting in the US, “it’s ok to go outside guys”.

9 JUN 2020:
Harvard Global Health Institute: “The WHO created confusion yesterday when it reported that asymptomatic patients rarely spread the disease,” an email from the Harvard Global Health Institute said Tuesday. “All of the best evidence suggests that people without symptoms can and do readily spread SARS-CoV-2, the virus that causes Covid-19. (Source)

• Scientists analysed data from over 28,000 Covid infections from 42 countries
• Cases were from towards the start of the pandemic in April 2020 up to July 2021
• They found asymptomatic people were less-likely to spread the virus to others
• Brits were urged in the pandemic to 'act like you've got it' and obey lockdowns

Glenn Beck Special First Aired November 17, 2021 regarding Covid19

⁣... not novel... no pandemic.. no variants... campaign of coercion & terror to address a stated objective. Dr David Martin, SG!! Who can tell us what the Vaxxed can do about this synthetic recombinant chimera protein? "There was no novel Coronavirus. Check of gene sequence vs all patent records showed not novel since 1999!

There are 120 patented pieces of evidence showing total fallacy of claim 'novel'!

Abstract

A helper cell for producing an infectious, replication defective, coronavirus (or more generally nidovirus) particle cell comprises (a) a nidovirus permissive cell; (b) a nidovirus replicon RNA comprising the nidovirus packaging signal and a heterologous RNA sequence, wherein the replicon RNA further lacks a sequence encoding at least one nidovirus structural protein; and (c) at least one separate helper RNA encoding the at least one structural protein absent from the replicon RNA, the helper RNA(s) lacking the nidovirus packaging signal. The combined expression of the replicon RNA and the helper RNA in the nidovirus permissive cell produces an assembled nidovirus particle which comprises the heterologous RNA sequence, is able to infect a cell, and is unable to complete viral replication in the absence of the helper RNA due to the absence of the structural protein coding sequence in the packaged replicon. Compositions for use in making such helper cells, along with viral particles produced from such cells, compositions of such viral particles, and methods of making and using such viral particles, are also disclosed.

Inventor: Kristopher M. Curtis, Boyd Yount, Ralph S. Baric
Current Assignee: University of North Carolina at Chapel Hill

[... Status ...]

2004-05-27 - Assigned to NORTH CAROLINA AT CHAPEL HILL, THE UNIVERSITY OF

[...]

2007-10-09 - Application granted

2007-10-09 - Publication of US7279327B2

2018-12-17 - Assigned to NATIONAL INSTITUTES OF HEALTH (NIH), U.S. DEPT. OF HEALTH AND HUMAN SERVICES (DHHS), U.S. GOVERNMENT

[...]

The present invention provides a live, attenuated coronavirus comprising a variant replicase gene encoding polyproteins comprising a mutation in one or more of non-structural protein(s) (nsp)-10, nsp-14, nsp-15 or nsp-16. The coronavirus may be used as a vaccine for treating and/or preventing a disease, such as infectious bronchitis, in a subject.

Inventor: Erica Bickerton, Sarah Keep, Paul Britton
Current Assignee: Pirbright Institute

[...]

Gammacoronavirus is a genus of animal virus belonging to the family Coronaviridae. Coronaviruses are enveloped viruses with a positive-sense single-stranded RNA genome and a helical symmetry.

[...]

Coronaviruses primarily infect the upper respiratory or gastrointestinal tract of mammals and birds. Five to six different currently known strains of coronaviruses infect humans. The most publicized human coronavirus, SARS-CoV which causes severe acute respiratory syndrome (SARS), has a unique pathogenesis because it causes both upper and lower respiratory tract infections and can also cause gastroenteritis. Middle East respiratory syndrome coronavirus (MERS-CoV) also causes a lower respiratory tract infection in humans. Coronaviruses are believed to cause a significant percentage of all common colds in human adults.

[...]

The variant replicase gene of the coronavirus of the present invention may be derived from an alphacoronavirus such as TGEV; a betacoronavirus such as MHV; or a gammacoronavirus such as IBV.

As used herein the term “derived from” means that the replicase gene comprises substantially the same nucleotide sequence as the wild-type replicase gene of the relevant coronavirus. For example, the variant replicase gene of the present invention may have up to 80%, 85%, 90%, 95%, 98% or 99% identity with the wild type replicase sequence. The variant coronavirus replicase gene encodes a protein comprising a mutation in one or more of non-structural protein (nsp)-10, nsp-14, nsp-15 or nsp-16 when compared to the wild-type sequence of the non-structural protein.

[...]

The virus isolated from the Dutch cases was identified by the Dutch Research Institute at Deventer as a new strain that they called D388. The Chinese connection came from further tests which showed that the virus was 99% similar to the Chinese QX viruses. A live attenuated QX-like IBV vaccine strain has now been developed.

IBV is an enveloped virus that replicates in the cell cytoplasm and contains an non-segmented, single-stranded, positive sense RNA genome. IBV has a 27.6 kb RNA genome and like all coronaviruses contains the four structural proteins; spike glycoprotein (S), small membrane protein (E), integral membrane protein (M) and nucleocapsid protein (N) which interacts with the genomic RNA.

The genome is organised in the following manner: 5′UTR—polymerase (replicase) gene—structural protein genes (S-E-M-N)—UTR 3′; where the UTR are untranslated regions (each ˜500 nucleotides in IBV).

[...]

Abstract

Disclosed herein is a newly isolated human coronavirus (SARS-CoV), the causative agent of severe acute respiratory syndrome (SARS). Also provided are the nucleic acid sequence of the SARS-CoV genome and the amino acid sequences of the SARS-CoV open reading frames, as well as methods of using these molecules to detect a SARS-CoV and detect infections therewith. Immune stimulatory compositions are also provided, along with methods of their use.

Inventor: Paul A. Rota, Larry J. Anderson, William J. Bellini, Cara Carthel Burns, Raymond Campagnoli, Qi ChenJames A. Comer, Shannon L. Emery, Dean D. Erdman, Cynthia S. Goldsmith, Charles D. Humphrey, Joseph P. Icenogle, Thomas G. Ksiazek, Stephan S. Monroe, William Allan Nix, M. Steven Oberste, Teresa C. T. Peret, Pierre E. Rollin, Mark A. Pallansch, Anthony Sanchez, Suxiang Tong, Sherif R. Zaki
Current Assignee: Centers of Disease Control and Prevention CDC

Abstract

Disclosed herein is a newly isolated human coronavirus (SARS-CoV), the causative agent of severe acute respiratory syndrome (SARS). Also provided are the nucleic acid sequence of the SARS-CoV genome and the amino acid sequences of the SARS-CoV open reading frames, as well as methods of using these molecules to detect a SARS-CoV and detect infections therewith. Immune stimulatory compositions are also provided, along with methods of their use.

[...]

Abstract

The invention provides compositions and methods that are useful for preventing and treating a coronavirus infection in a subject. More specifically, the invention provides peptides and conjugates and pharmaceutical compositions containing those peptides and conjugates that block fusion of a coronavirus, such as the SARS virus, to a target cell. This blocking mechanism prevents or treats a coronavirus infection, such as a SARS infection, in a subject, such as a human subject.

Inventor: John W. Erickson, Abelardo Silva
Current Assignee: Sequoia Pharmaceuticals Inc

Abstract

The present invention relates in part to amino acid sequences that are directed against and/or that can specifically bind to an envelope protein of a virus, as well as to compounds or constructs, and in particular proteins and polypeptides, that comprise or essentially consist of one or more such amino acid sequences.

Inventor: Anna Hultberg, Bram Maassen, Peter Vanlandschoot, Erik DeplaCatelijne Stortelers, Cornelis Theodorus Verrips, Steven Van Gucht, Jose Melero, Michael John Scott Saunders, Johannes Joseph Wilhelmus de Haard, Robert Anthony Weiss, Nigel J. Temperton, Xavier Saelens, Bert Schepens, Alexander Szyroki, Michael Marie Harmsen
Current Assignee: Ablynx NV

Abstract

An outbreak of a virulent respiratory virus, now known as Severe Acute Respiratory Syndrome (SARS), was identified in Hong Kong, China and a growing number of countries around the world in 2003. The invention relates to nucleic acids and proteins from the SARS coronavirus. These nucleic acids and proteins can be used in the preparation and manufacture of vaccine formulations, diagnostic reagents, kits, etc. The invention also provides methods for treating SARS by administering small molecule antiviral compounds, as well as methods of identifying potent small molecules for the treatment of SARS.

Inventor: Rino Rappuoli, Vega Masignani, Konrad Stadler, Jens Gregersen, David ChienJang Han, John Polo, Amy Weiner ,Michael Houghton, Hyun Song, Mi-Young Seo, John Donnelly, Hans Klenk, Nicholas Valiante

Current Assignee: GlaxoSmithKline Biologicals SA

Abstract

The invention relates to the spike protein from the virus (SARS-CoV) that is etiologically linked to severe acute respiratory syndrome (SARS); polypeptides and peptide fragments of the spike protein; nucleic acid segments and constructs that encode the spike protein, polypeptides and peptide fragments of the spike protein, and coupled proteins that include the spike protein or a portion thereof; peptidomimetics; vaccines; methods for vaccination and treatment of severe acute respiratory syndrome; antibodies; aptamers; and kits containing immunological compositions, or antibodies (or aptamers) that bind to the spike protein.

Inventor: Dimiter Dimitrov, Xiaodong Xiao, Zhu Zhongyu

Assigned to: US Department of Health and Human Services

Status: Abandoned

A list of patents linked to specific diseases and viruses is being shared with the suggestion that it is proof that viruses are manmade. This is false, and a misinterpretation of the types of patent listed.

[...]

Abstract

Emerging infectious diseases, such as severe acute respiratory syndrome (SARS) and Zika virus disease, present a major threat to public health^1–3. Despite intense research efforts, how, when and where new diseases appear are still a source of considerable uncertainty. A severe respiratory disease was recently reported in Wuhan, Hubei province, China. As of 25 January 2020, at least 1,975 cases had been reported since the first patient was hospitalized on 12 December 2019. Epidemiological investigations have suggested that the outbreak was associated with a seafood market in Wuhan. Here we study a single patient who was a worker at the market and who was admitted to the Central Hospital of Wuhan on 26 December 2019 while experiencing a severe respiratory syndrome that included fever, dizziness and a cough. Metagenomic RNA sequencing⁴ of a sample of bronchoalveolar lavage fluid from the patient identified a new RNA virus strain from the family Coronaviridae, which is designated here ‘WH-Human 1’ coronavirus (and has also been referred to as ‘2019-nCoV’). Phylogenetic analysis of the complete viral genome (29,903 nucleotides) revealed that the virus was most closely related (89.1% nucleotide similarity) to a group of SARS-like coronaviruses (genus Betacoronavirus, subgenus Sarbecovirus) that had previously been found in bats in China⁵. This outbreak highlights the ongoing ability of viral spill-over from animals to cause severe disease in humans.

NCBI Reference Sequence: NC_045512.2

DEFINITION Severe acute respiratory syndrome coronavirus 2 isolate Wuhan-Hu-1,
 complete genome.

[...]

DEFINITION Severe acute respiratory syndrome coronavirus 2 isolate Wuhan-Hu-1, complete genome.

BLAST finds regions of similarity between biological sequences. The program compares nucleotide or protein sequences to sequence databases and calculates the statistical significance.

In early 2020, a few months after the Covid-19 pandemic began, scientists were able to sequence the full genome of SARS-CoV-2, the virus that causes the Covid-19 infection. While many of its genes were already known at that point, the full complement of protein-coding genes was unresolved.

Now, after performing an extensive comparative genomics study, MIT researchers have generated what they describe as the most accurate and complete gene annotation of the SARS-CoV-2 genome. In their study, which appears today in Nature Communications, they confirmed several protein-coding genes and found that a few others that had been suggested as genes do not code for any proteins.

“We were able to use this powerful comparative genomics approach for evolutionary signatures to discover the true functional protein-coding content of this enormously important genome,” says Manolis Kellis, who is the senior author of the study and a professor of computer science in MIT’s Computer Science and Artificial Intelligence Laboratory (CSAIL) as well as a member of the Broad Institute of MIT and Harvard.

Biologists from the Applied Physics Lab work to track the mutation of SARS-CoV-2, the virus that causes COVID-19

[...]

"When this virus was first sequenced in China, that information was helpful in starting the process to develop a vaccine," Thielen explained. "What we're doing informs whether or not the virus is mutating away from that original sequence, and how quickly. Based on the mutation rate, early data indicates that this would likely be a single vaccine rather than one that needs to be updated each year, like the flu shot."

What is genomic sequencing and why is it important to understand the genomic sequence of COVID-19?

Thielen: Genomic sequencing is a technique that allows us to read and interpret genetic information found within DNA or RNA. When we look at virus genome sequences from patient samples that test positive for COVID-19, we're interested in understanding where their version of the virus originated. For example, does the virus look similar to how it looks in Washington State? Or in New York? Or in Europe? Right now, we're working to analyze many genome sequences from SARS-CoV-2, the virus that causes COVID-19, that are circulating in the Baltimore area and in Maryland. Our goal is to understand how the virus is evolving as it spreads. So far, there are over 1,000 COVID-19 genomes that have been published worldwide.

A guide to implementation for maximum impact on public health

[...]

5.1.1 Identifying the causative agent of COVID-19

SARS-CoV-2 was independently identified and sequenced in early 2020 by Wu et al., Lu et al. and Zhou et al. (52, 59,60). Several different metagenomic next-generation sequencing (mNGS) approaches were used to identify the causative pathogen of COVID-19. Metagenomic sequencing permits untargeted sequencing of nucleic acid in a sample, and can therefore identify viral RNA or DNA if present at high enough copy numbers relative to DNA or RNA from other sources (see also section 6.5.1). Completion of the full-length virus genome sequences, including the genome termini, generally involved Sanger sequencing and a 5’/3’ rapid amplification of cDNA ends (RACE) method. This method is cost-efficient for sequencing short regions of a genome that may be missed with metagenomic methods, but relies on previous knowledge of the sequence information relatively close to the missing region.

[...]

5.2.1 Host receptor usage

Since viruses can replicate only inside the living cells of a host organism, determining the host cellular receptor used by SARS-CoV-2 is essential to understanding its basic biology. Receptor binding is mediated by the S protein of the virus. Genetic similarities in the S protein receptorbinding motif between SARS-CoV-2 and other, previously investigated coronaviruses have helped to identify the cellular receptor to which SARS-CoV-2 binds, and hence the cell types that it might infect. Initial studies indicated that SARS-CoV-2 was likely to use the same angiotensin-converting enzyme 2 (ACE2) cell receptor as the 2002–2003 SARS-CoV, and was likely to bind to this receptor with high affinity (70, 71). Most amino acid residues that are known to be essential for ACE2 binding by SARS-CoV are conserved in SARS-CoV-2 (70). In vitro assays confirm the strong specificity for ACE2 suggested by direct structural studies (72).

The spike glycoprotein of the newly emerged SARS-CoV-2 contains a potential cleavage site for furin proteases. This observation has implications for the zoonotic origin of the virus and its epidemic spread in China.

The membrane of coronaviruses harbors a trimeric transmembrane spike (S) glycoprotein (pictured) which is essential for entry of virus particles into the cell. The S protein contains two functional domains: a receptor binding domain, and a second domain which contains sequences that mediate fusion of the viral and cell membranes. The S glycoprotein must be cleaved by cell proteases to enable exposure of the fusion sequences and hence is needed for cell entry.

The nature of the cell protease that cleaves the S glycoprotein varies according to the coronavirus. The MERS-CoV S glycoprotein contains a furin cleavage site and is probably processed by these intracellular proteases during exit from the cell. The virus particles are therefore ready for entry into the next cell. In contrast, the SARS-CoV S glycoprotein is uncleaved upon virus release from cells; it is likely cleaved during virus entry into a cell.

Proteolytic cleavage of the S glycoprotein can determine whether the virus can cross species, e.g. from bats to humans. For example, the S glycoprotein from a MERS-like CoV from Ugandan bats can bind to human cells but cannot mediate virus entry. However, if the protease trypsin is included during infection, the S glycoprotein is cleaved and virus entry takes place. This observation demonstrates that cleavage of the S glycoprotein is a barrier to zoonotic coronavirus transmission.

[...]

Abstract

SARS-CoV-2 has resulted in a global pandemic and shutdown economies around the world. Sequence analysis indicates that the novel coronavirus (CoV) has an insertion of a furin cleavage site (PRRAR) in its spike protein. Absent in other group 2B CoVs, the insertion may be a key factor in the replication and virulence of SARS-CoV-2. To explore this question, we generated a SARS-CoV-2 mutant lacking the furin cleavage site (ΔPRRA) in the spike protein. This mutant virus replicated with faster kinetics and improved fitness in Vero E6 cells. The mutant virus also had reduced spike protein processing as compared to wild-type SARS-CoV-2. In contrast, the ΔPRRA had reduced replication in Calu3 cells, a human respiratory cell line, and had attenuated disease in a hamster pathogenesis model. Despite the reduced disease, the ΔPRRA mutant offered robust protection from SARS-CoV-2 rechallenge. Importantly, plaque reduction neutralization tests (PRNT ₅₀ ) with COVID-19 patient sera and monoclonal antibodies against the receptor-binding domain found a shift, with the mutant virus resulting in consistently reduced PRNT ₅₀ titers. Together, these results demonstrate a critical role for the furin cleavage site insertion in SARS-CoV-2 replication and pathogenesis. In addition, these findings illustrate the importance of this insertion in evaluating neutralization and other downstream SARS-CoV-2 assays.

Importance: As COVID-19 has impacted the world, understanding how SARS-CoV-2 replicates and causes virulence offers potential pathways to disrupt its disease. By removing the furin cleavage site, we demonstrate the importance of this insertion to SARS-CoV-2 replication and pathogenesis. In addition, the findings with Vero cells indicate the likelihood of cell culture adaptations in virus stocks that can influence reagent generation and interpretation of a wide range of data including neutralization and drug efficacy. Overall, our work highlights the importance of this key motif in SARS-CoV-2 infection and pathogenesis.

Article summary: A deletion of the furin cleavage site in SARS-CoV-2 amplifies replication in Vero cells, but attenuates replication in respiratory cells and pathogenesis in vivo. Loss of the furin site also reduces susceptibility to neutralization in vitro .

LA JOLLA—Scientists have known for a while that SARS-CoV-2’s distinctive “spike” proteins help the virus infect its host by latching on to healthy cells. Now, a major new study shows that the virus spike proteins (which behave very differently than those safely encoded by vaccines) also play a key role in the disease itself.

The paper, published on April 30, 2021, in Circulation Research, also shows conclusively that COVID-19 is a vascular disease, demonstrating exactly how the SARS-CoV-2 virus damages and attacks the vascular system on a cellular level. The findings help explain COVID-19’s wide variety of seemingly unconnected complications, and could open the door for new research into more effective therapies.

“A lot of people think of it as a respiratory disease, but it’s really a vascular disease,” says Assistant Research Professor Uri Manor, who is co-senior author of the study. “That could explain why some people have strokes, and why some people have issues in other parts of the body. The commonality between them is that they all have vascular underpinnings.”

The following article was published by Salk Institute on April 30, 2021. It reports on a study funded by a number of health organizations, including the National Institutes of Health which discovered that SARS-CoV-2 is in fact a vascular disease, not a respiratory disease.

According to the study, the SARS-CoV-2’s spike protein damages and attacks the vascular system on a cellular level. The researchers believe that explains the wide variety of seemingly unconnected complications related to COVID-19.

Taking the study deeper, the researchers created a “pseudovirus” that was surrounded by SARS-CoV-2 classic crown of spike proteins, but did not contain the actual virus. They found that “exposure to this pseudovirus resulted in damage to the lungs and arteries of an animal model – proving that the spike protein alone was enough to cause the disease”.

[...]

Abstract

Antibodies against the receptor-binding domain (RBD) of the SARS-CoV-2 spike protein prevent SARS-CoV-2 infection. However, the effects of antibodies against other spike protein domains are largely unknown. Here, we screened a series of anti-spike monoclonal antibodies from coronavirus disease 2019 (COVID-19) patients and found that some of antibodies against the N-terminal domain (NTD) induced the open conformation of RBD and thus enhanced the binding capacity of the spike protein to ACE2 and infectivity of SARS-CoV-2. Mutational analysis revealed that all of the infectivity-enhancing antibodies recognized a specific site on the NTD. Structural analysis demonstrated that all infectivity-enhancing antibodies bound to NTD in a similar manner. The antibodies against this infectivity-enhancing site were detected at high levels in severe patients. Moreover, we identified antibodies against the infectivity-enhancing site in uninfected donors, albeit at a lower frequency. These findings demonstrate that not only neutralizing antibodies but also enhancing antibodies are produced during SARS-CoV-2 infection.

Abstract

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes a broad range of clinical responses including prominent microvascular damage. The capacity of SARS-CoV-2 to infect vascular cells is still debated. Additionally, the SARS-CoV-2 Spike (S) protein may act as a ligand to induce non-infective cellular stress. We tested this hypothesis in pericytes (PCs), which are reportedly reduced in the heart of patients with severe coronavirus disease-2019 (COVID-19). Here we newly show that the in vitro exposure of primary human cardiac PCs to the SARS-CoV-2 wildtype strain or the α and δ variants caused rare infection events. Exposure to the recombinant S protein alone elicited signalling and functional alterations, including: (1) increased migration, (2) reduced ability to support endothelial cell (EC) network formation on Matrigel, (3) secretion of pro-inflammatory molecules typically involved in the cytokine storm, and (4) production of pro-apoptotic factors causing EC death. Next, adopting a blocking strategy against the S protein receptors angiotensin-converting enzyme 2 (ACE2) and CD147, we discovered that the S protein stimulates the phosphorylation/activation of the extracellular signal-regulated kinase 1/2 (ERK1/2) through the CD147 receptor, but not ACE2, in PCs. The neutralisation of CD147, either using a blocking antibody or mRNA silencing, reduced ERK1/2 activation, and rescued PC function in the presence of the S protein. Immunoreactive S protein was detected in the peripheral blood of infected patients. In conclusion, our findings suggest that the S protein may prompt PC dysfunction, potentially contributing to microvascular injury. This mechanism may have clinical and therapeutic implications.

Abstract

Acute lung injury (ALI) leading to acute respiratory distress syndrome is the major cause of COVID-19 lethality. Cell entry of SARS-CoV-2 occurs via the interaction between its surface spike protein (SP) and angiotensin-converting enzyme-2 (ACE2). It is unknown if the viral spike protein alone is capable of altering lung vascular permeability in the lungs or producing lung injury in vivo. To that end, we intratracheally instilled the S1 subunit of SARS-CoV-2 spike protein (S1SP) in K18-hACE2 transgenic mice that overexpress human ACE2 and examined signs of COVID-19-associated lung injury 72 h later. Controls included K18-hACE2 mice that received saline or the intact SP and wild-type (WT) mice that received S1SP. K18-hACE2 mice instilled with S1SP exhibited a decline in body weight, dramatically increased white blood cells and protein concentrations in bronchoalveolar lavage fluid (BALF), upregulation of multiple inflammatory cytokines in BALF and serum, histological evidence of lung injury, and activation of signal transducer and activator of transcription 3 (STAT3) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathways in the lung. K18-hACE2 mice that received either saline or SP exhibited little or no evidence of lung injury. WT mice that received S1SP exhibited a milder form of COVID-19 symptoms, compared with the K18-hACE2 mice. Furthermore, S1SP, but not SP, decreased cultured human pulmonary microvascular transendothelial resistance (TER) and barrier function. This is the first demonstration of a COVID-19-like response by an essential virus-encoded protein by SARS-CoV-2 in vivo. This model of COVID-19-induced ALI may assist in the investigation of new therapeutic approaches for the management of COVID-19 and other coronaviruses.

Abstract

Human prion protein and prion-like protein misfolding are widely recognized as playing a causal role in many neurodegenerative diseases. Based on in vitro and in vivo experimental evidence relating to prion and prion-like disease, we extrapolate from the compelling evidence that the spike glycoprotein of SARS-CoV-2 contains extended amino acid sequences characteristic of a prion-like protein to infer its potential to cause neurodegenerative disease. We propose that vaccine-induced spike protein synthesis can facilitate the accumulation of toxic prion-like fibrils in neurons. We outline various pathways through which these proteins could be expected to distribute throughout the body. We review both cellular pathologies and the expression of disease that could become more frequent in those who have undergone mRNA vaccination. Specifically, we describe the spike protein’s contributions, via its prion-like properties, to neuroinflammation and neurodegenerative diseases; to clotting disorders within the vasculature; to further disease risk due to suppressed prion protein regulation in the context of widely prevalent insulin resistance; and to other health complications. We explain why these prion-like characteristics are more relevant to vaccine-related mRNA-induced spike proteins than natural infection with SARS-CoV-2. We note with an optimism an apparent loss of prion-like properties among the current Omicron variants. We acknowledge that the chain of pathological events described throughout this paper is only hypothetical and not yet verified. We also acknowledge that the evidence we usher in, while grounded in the research literature, is currently largely circumstantial, not direct. Finally, we describe the implications of our findings for the general public, and we briefly discuss public health recommendations we feel need urgent consideration.

An earlier version of this article was previously posted to the Authorea preprint server on August 16, 2022.

Abstract

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused the pandemic of the coronavirus induced disease 2019 (COVID-19) with evolving variants of concern. It remains urgent to identify novel approaches against broad strains of SARS-CoV-2, which infect host cells via the entry receptor angiotensin-converting enzyme 2 (ACE2). Herein, we report an increase in circulating extracellular vesicles (EVs) that express ACE2 (evACE2) in plasma of COVID-19 patients, which levels are associated with severe pathogenesis. Importantly, evACE2 isolated from human plasma or cells neutralizes SARS-CoV-2 infection by competing with cellular ACE2. Compared to vesicle-free recombinant human ACE2 (rhACE2), evACE2 shows a 135-fold higher potency in blocking the binding of the viral spike protein RBD, and a 60- to 80-fold higher efficacy in preventing infections by both pseudotyped and authentic SARS-CoV-2. Consistently, evACE2 protects the hACE2 transgenic mice from SARS-CoV-2-induced lung injury and mortality. Furthermore, evACE2 inhibits the infection of SARS-CoV-2 variants (α, β, and δ) with equal or higher potency than for the wildtype strain, supporting a broad-spectrum antiviral mechanism of evACE2 for therapeutic development to block the infection of existing and future coronaviruses that use the ACE2 receptor.

ABSTRACT

The recent COVID-19 pandemic is a treatment challenge in the acute infection stage but the recognition of chronic COVID-19 symptoms termed post-acute sequelae SARS-CoV-2 infection (PASC) may affect up to 30% of all infected individuals. The underlying mechanism and source of this distinct immunologic condition three months or more after initial infection remains elusive. Here, we investigated the presence of SARS-CoV-2 S1 protein in 46 individuals. We analyzed T-cell, B-cell, and monocytic subsets in both severe COVID-19 patients and in patients with post-acute sequelae of COVID-19 (PASC). The levels of both intermediate (CD14+, CD16+) and non-classical monocyte (CD14Lo, CD16+) were significantly elevated in PASC patients up to 15 months post-acute infection compared to healthy controls (P=0.002 and P=0.01, respectively). A statistically significant number of non-classical monocytes contained SARS-CoV-2 S1 protein in both severe (P=0.004) and PASC patients (P=0.02) out to 15 months post-infection. Non-classical monocytes were sorted from PASC patients using flow cytometric sorting and the SARS-CoV-2 S1 protein was confirmed by mass spectrometry. Cells from 4 out of 11 severe COVID-19 patients and 1 out of 26 also contained SARS-CoV-2 RNA. Non-classical monocytes are capable of causing inflammation throughout the body in response to fractalkine/CX3CL1 and RANTES/CCR5.

ABSTRACT

SARS-CoV-2, the causative agent of COVID-19 disease, has resulted in the death of millions worldwide since the beginning of the pandemic in December 2019. While much progress has been made to understand acute manifestations of SARS-CoV-2 infection, less is known about post-acute sequelae of COVID-19 (PASC). We investigated the levels of both Spike protein (Spike) and viral RNA circulating in patients hospitalized with acute COVID-19 and in patients with and without PASC. We found that Spike and viral RNA were more likely to be present in patients with PASC. Among these patients, 30% were positive for both Spike and viral RNA; whereas, none of the individuals without PASC were positive for both. The levels of Spike and/or viral RNA in the PASC+ve patients were found to be increased or remained the same as in the acute phase; whereas, in the PASC−ve group, these viral components decreased or were totally absent. Additionally, this is the first report to show that part of the circulating Spike is linked to extracellular vesicles without any presence of viral RNA in these vesicles. In conclusion, our findings suggest that Spike and/or viral RNA fragments persist in the recovered COVID-19 patients with PASC up to 1 year or longer after acute SARS-CoV-2 infection.

Abstract

The diagnosis of postacute sequelae of coronavirus disease 2019 (PASC) poses an ongoing medical challenge. To identify biomarkers associated with PASC we analyzed plasma samples collected from PASC and coronavirus disease 2019 patients to quantify viral antigens and inflammatory markers. We detect severe acute respiratory syndrome coronavirus 2 spike predominantly in PASC patients up to 12 months after diagnosis.

In this two-part paper, we aim to give an overview on COVID-19 related abnormal blood clots, how they form, how to detect them early, and how they're being treated

Strange Clots

Since mid-2021, unusual, lengthy blood clots found in the vessels of COVID-19 patients and jab recipients have been reported across the world.

“We as embalmers are seeing some strange clots since the COVID outbreak. These clots are very rubbery feeling and very long as they exit the veins that we use during the embalming procedure. They really appear to be like earthworms. I have never seen this in my career until now,” Larry Mills, a licensed embalmer and funeral director in the State of Alabama, told The Epoch Times.

Other embalmers confirmed similar findings and spoke on the condition of anonymity.

Richard Hirschman, Alabama funeral director and embalmer since 2001, was one of the first to bring attention to this phenomenon. He said that prior to COVID perhaps 5 to 10 percent of people had these clots. Now more than half of the bodies he sees have them.

One embalmer, licensed since 2001, said in an interview, “I can tell you with certainty that the clots Richard has shown online are a phenomenon that I have not witnessed until probably the middle of last year. That is pretty much all I have to say about it. I have no knowledge as to what is causing the clots, but they did seemingly start showing up around the middle of 2021.”

[...]

Abstract

The pathophysiology of COVID-19-associated coagulopathy is complex and not fully understood. SARS-CoV-2 spike protein (SP) may activate platelets and interact with fibrin(ogen). We aimed to investigate whether isolated SP can be present in clots retrieved in COVID-19 patients with acute ischemic stroke (by mechanical thrombectomy) and myocardial infarction. In this pilot study, we could detect SP, but not nucleocapsid protein, on platelets of COVID-19 patients’ thrombi. In addition, in all three COVID-19 thrombi analyzed for molecular biology, no SARS-CoV-2 RNA could be detected by real-time polymerase chain reaction. These data could support the hypothesis that free SP, besides the whole virus, may be the trigger of platelet activation and clot formation in COVID-19.

Virus entry into animal cells is initiated by attachment to target macromolecules located on host cells. The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) trimeric spike glycoprotein targets host angiotensin converting enzyme 2 to gain cellular access. The SARS-CoV-2 glycoprotein contains a neurotoxin-like region that has sequence similarities to the rabies virus and the HIV glycoproteins, as well as to snake neurotoxins, which interact with nicotinic acetylcholine receptor (nAChR) subtypes via this region. Using a peptide of the neurotoxin-like region of SARS-CoV-2 (SARS-CoV-2 glycoprotein peptide [SCoV2P]), we identified that this area moderately inhibits α3β2, α3β4, and α4β2 subtypes, while potentiating and inhibiting α7 nAChRs. These nAChR subtypes are found in target tissues including the nose, lung, central nervous system, and immune cells. Importantly, SCoV2P potentiates and inhibits ACh-induced α7 nAChR responses by an allosteric mechanism, with nicotine enhancing these effects. Live-cell confocal microscopy was used to confirm that SCoV2P interacts with α7 nAChRs in transfected neuronal-like N2a and human embryonic kidney 293 cells. The SARS-CoV-2 ectodomain functionally potentiates and inhibits the α7 subtype with nanomolar potency. Our functional findings identify that the α7 nAChR is a target for the SARS-CoV-2 glycoprotein, providing a new aspect to our understanding of SARS-CoV-2 and host cell interactions, in addition to disease pathogenesis.

[...]

SARS induced Death in mice via dysfunction of the Medulla via the OLFACTORY NERVE

Viral antigen distribution in the brain following intranasal inoculation. Brains were harvested from mice infected intranasally with 2.4 × 104 PFU and stained for viral antigen. (A to C) Antigen distribution in the brain at 60 h (A) and 3 (B), 4 (C), and 5 (D) days p.i. (E to J) The brain stem (E, G, and I) and hypothalamus (F, H, and J) were examined for viral antigen and inflammation. (E and F) Naïve controls. (G and H) SARS-CoV-infected brains exhibited antigen exclusively in neurons with no obvious inflammation at day 6 p.i. (compare to naïve controls). (I and J) JHMV-infected brains showed less extensive neuronal infection but severe perivascular inflammation (closed arrows) and meningitis (open arrows) at day 6 p.i. Original magnifications: ×1 (A to D) and ×5 (E to J).

Why this has not previously come to light and been discussed is beyond me. As you know, I have been researching the demyelination hypothesis as the cause of the Sudden Cardiac Deaths. I have discovered that the original SARS was able to induce Neuronal Death in the Medulla (cardiorespiratory center) resulting in the death of the subject.

[...]

Abstract

The COVID-19 pandemic caused much illness, many deaths, and profound disruption to society. The production of 'safe and effective' vaccines was a key public health target. Sadly, unprecedented high rates of adverse events have overshadowed the benefits. This two-part narrative review presents evidence for the widespread harms of novel product COVID-19 mRNA and adenovectorDNA vaccines and is novel in attempting to provide a thorough overview of harms arising from the new technology in vaccines that relied on human cells producing a foreign antigen that has evidence of pathogenicity. This first paper explores peer-reviewed data counter to the 'safe and effective' narrative attached to these new technologies. Spike protein pathogenicity, termed 'spikeopathy', whether from the SARS-CoV-2 virus or produced by vaccine gene codes, akin to a 'synthetic virus', is increasingly understood in terms of molecular biology and pathophysiology. Pharmacokinetic transfection through body tissues distant from the injection site by lipid-nanoparticles or viral-vector carriers means that 'spikeopathy' can affect many organs. The inflammatory properties of the nanoparticles used to ferry mRNA; N1-methylpseudouridine employed to prolong synthetic mRNA function; the widespread biodistribution of the mRNA and DNA codes and translated spike proteins, and autoimmunity via human production of foreign proteins, contribute to harmful effects. This paper reviews autoimmune, cardiovascular, neurological, potential oncological effects, and autopsy evidence for spikeopathy. With many gene-based therapeutic technologies planned, a re-evaluation is necessary and timely.

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has led to the coronavirus disease 2019 (COVID-19) pandemic, severely affecting public health and the global economy. Adaptive immunity plays a crucial role in fighting against SARS-CoV-2 infection and directly influences the clinical outcomes of patients. Clinical studies have indicated that patients with severe COVID-19 exhibit delayed and weak adaptive immune responses; however, the mechanism by which SARS-CoV-2 impedes adaptive immunity remains unclear. Here, by using an in vitro cell line, we report that the SARS-CoV-2 spike protein significantly inhibits DNA damage repair, which is required for effective V(D)J recombination in adaptive immunity. Mechanistically, we found that the spike protein localizes in the nucleus and inhibits DNA damage repair by impeding key DNA repair protein BRCA1 and 53BP1 recruitment to the damage site. Our findings reveal a potential molecular mechanism by which the spike protein might impede adaptive immunity and underscore the potential side effects of full-length spike-based vaccines.

Abstract

The recently identified, globally predominant SARS-CoV-2 Omicron variant (BA.1) is highly transmissible, even in fully vaccinated individuals, and causes attenuated disease compared with other major viral variants recognized to date. The Omicron spike (S) protein, with an unusually large number of mutations, is considered the major driver of these phenotypes. We generated chimeric recombinant SARS-CoV-2 encoding the S gene of Omicron in the backbone of an ancestral SARS-CoV-2 isolate and compared this virus with the naturally circulating Omicron variant. The Omicron S-bearing virus robustly escapes vaccine-induced humoral immunity, mainly due to mutations in the receptor binding motif (RBM), yet unlike naturally occurring Omicron, efficiently replicates in cell lines and primary-like distal lung cells. In K18-hACE2 mice, while Omicron causes mild, non-fatal infection, the Omicron S-carrying virus inflicts severe disease with a mortality rate of 80%. This indicates that while the vaccine escape of Omicron is defined by mutations in S, major determinants of viral pathogenicity reside outside of S.

[...]

• Researchers added Omicron's spike protein to the original Wuhan Covid strain
• Omicron's spike is highly mutated which made it the most infectious variant ever
• Eight in 10 mice infected with the lab-created strain died at Boston University lab

Boston University scientists were today condemned for 'playing with fire' after it emerged they had created a lethal new Covid strain in a laboratory.

DailyMail.com revealed the team had made a hybrid virus — combining Omicron and the original Wuhan strain — that killed 80 per cent of mice in a study.

The revelation exposes how dangerous virus manipulation research continues to go on even in the US, despite fears similar practices may have started the pandemic.

Professor Shmuel Shapira, a leading scientist in the Israeli Government, said: 'This should be totally forbidden, it's playing with fire.'

Gain of function research - when viruses are purposefully manipulated to be more infectious or deadly - is thought to be at the center of Covid's origin.

A Chinese laboratory located just miles from the first cluster of cases carried out similar research on bat coronaviruses.

But the practice has been largely restricted in the US since 2017. 

Dr Richard Ebright, a chemist at Rutgers University in New Brunswick, New Jersey, told DailyMail.com that: 'The research is a clear example of gain of function research.

He added: 'If we are to avoid a next lab-generated pandemic, it is imperative that oversight of enhanced potential pandemic pathogen research be strengthened.'

[...]

According to a new paper just made public, researchers at Boston University were able to combine the spike protein from Omicron with the original strain of the virus, to create a new chimera strain that was so deadly it killed 80 percent of the humanized mice that they were testing on.

Using grant funding from both the NIH and the NIAID, the sub-agency led by Dr. Anthony Fauci, these scientists were able to cobble together a new strain of COVID. They dubbed their new creation Omicron S.

[...]

Boston University issued a statement Tuesday defending its research of a COVID-19 Omicron strain when they took the variant’s spike protein and attached it to the original COVID-19 strain, leading to a higher mortality rate in a certain species of mice, triggering concern among lawmakers.

“The Omicron S-bearing virus robustly escapes vaccine-induced humoral immunity, mainly due to mutations in the receptor-binding motif… while Omicron causes mild, non-fatal infection, the Omicron S-carrying virus inflicts severe disease with a mortality rate of 80 percent,” the preprint study said.

One lawmaker, Sen. Roger Marshall (R-Kan.), said that the research entailed “lethal gain of function virus research” that creates the “potential to kill more people than any singular nuclear weapon.” Marshal, a doctor, added that “viruses have managed to escape even the most secure labs” and said such “research must stop immediately while the risks and benefits can be investigated.”

Meanwhile, Emily Erbelding, director of the National Institute of Allergy and Infectious Diseases’s division of microbiology and infectious diseases, told Stat News that the Boston University’s grant application didn’t specify that researchers wanted to perform this work and the group did not say it was performing experiments to possible enhance a COVID-19 variant. An investigation is now underway, she said.

Boston University issued a lengthy statement defending its research and said critics have misrepresented the goals of the study while refuting allegations that the study involved gain-of-function research, which can make a pathogen more deadly or transmissible.

“The research was reviewed and approved by the Institutional Biosafety Committee (IBC), which consists of scientists as well as local community members,” the statement from Boston University said. “The Boston Public Health Commission also approved the research. Furthermore, this research mirrors and reinforces the findings of other, similar research performed by other organizations, including the FDA. Ultimately, this research will provide a public benefit by leading to better, targeted therapeutic interventions to help fight against future pandemics.”

Certain reports about the study were “false and inaccurate,” Boston University official Ronald Corley said in a statement. A report from the Daily Mail, he alleged, took the “80 percent” line out of context.

“We want to address the false and inaccurate reporting about Boston University COVID-19 research, which appeared today in the Daily Mail,” said the statement. “First, this research is not gain-of-function research, meaning it did not amplify the Washington state SARS-CoV-2 virus strain or make it more dangerous. In fact, this research made the virus replicate less dangerous.”

Lab Escape?

Addressing concerns that the manipulated COVID-19 Omicron strain could escape Boston University’s laboratory, Corley said the school takes safety seriously.

“We take our safety and security of how we handle pathogens seriously, and the virus does not leave the laboratory in which it’s being studied,” he said. “Our whole goal is for the public’s health. And this study was part of that, finding what part of the virus is responsible for causing severe disease. If we can understand that, we can then develop the tools that we need to develop better therapeutics.”

However, one doctor interviewed by the Daily Mail expressed alarm over the research.

“The issue is what you’re going to be using [the labs] for. If they’re for diagnostic purposes, then you need them. But I don’t think every country needs a BSL-4,” Dr. Paul Hunter, an expert in infectious diseases at England’s University of East Anglia, said, referring to the top level of biosecurity used in laboratories.

“If they start having a dual purpose for research that has offensive military implications, that is the concern,” he said.

[...]

Abstract

The COVID-19 pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has resulted in over 6 million deaths worldwide. The high variability in COVID-19 symptoms remains one of the most interesting mysteries of the pandemic. Genetic and environmental factors are likely to be key determinants of COVID-19 symptomatology. Here, we explored ACE2 as a genetic determinant for SARS-CoV-2 infection and COVID-19 symptomatology. Each human genome encodes two alleles of ACE2, which encodes the cell entry receptor for SARS-CoV-2. Here, we determined whether naturally occurring human ACE2 (hACE2) polymorphisms in the human population affect SARS-CoV-2 infection and the severity of COVID-19 symptoms. ACE2 variants S19P, I21V, E23K, K26R, K31R, N33I, H34R, E35K, and T92I showed increased virus infection compared to wild-type ACE2; thus, these variants could increase the risk for COVID-19. In contrast, variants D38V, Y83H, I468V, and N638S showed reduced infection, indicating a potential protective effect. hACE2 variants K26R and T92I increased infection by three-fold without changing the levels of ACE2 on the surface of the cells, suggesting that these variants may increase the risk of severe COVID-19. On the contrary, hACE2 variants D38V and Y83H decreased SARS-CoV-2 infection by four- and ten-fold, respectively, without changing surface expression, suggesting that these variants may protect against severe COVID-19. Remarkably, all protective hACE2 Polymorphisms were found almost exclusively in Asian populations, which may provide a partial explanation for the low COVID-19 mortality rates in Asian countries. Thus, hACE2 polymorphisms may modulate susceptibility to SARS-CoV-2 in the host and partially account for the differences in severity of COVID-19 among different ethnic groups.

Abstract

Background: Coronavirus Disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has now been confirmed worldwide. Yet, COVID-19 is strangely and tragically selective. Morbidity and mortality due to COVID19 rise dramatically with age and co-existing health conditions, including cancer and cardiovascular diseases. Human genetic factors may contribute to the extremely high transmissibility of SARS-CoV-2 and to the relentlessly progressive disease observed in a small but significant proportion of infected individuals, but these factors are largely unknown.

Main body: In this study, we investigated genetic susceptibility to COVID-19 by examining DNA polymorphisms in ACE2 and TMPRSS2 (two key host factors of SARS-CoV-2) from ~ 81,000 human genomes. We found unique genetic susceptibility across different populations in ACE2 and TMPRSS2. Specifically, ACE2 polymorphisms were found to be associated with cardiovascular and pulmonary conditions by altering the angiotensinogen-ACE2 interactions, such as p.Arg514Gly in the African/African-American population. Unique but prevalent polymorphisms (including p.Val160Met (rs12329760), an expression quantitative trait locus (eQTL)) in TMPRSS2, offer potential explanations for differential genetic susceptibility to COVID-19 as well as for risk factors, including those with cancer and the high-risk group of male patients. We further discussed that polymorphisms in ACE2 or TMPRSS2 could guide effective treatments (i.e., hydroxychloroquine and camostat) for COVID-19.

Conclusion: This study suggested that ACE2 or TMPRSS2 DNA polymorphisms were likely associated with genetic susceptibility of COVID-19, which calls for a human genetics initiative for fighting the COVID-19 pandemic.

[...]

ACE2 polymorphism analysis across different populations

[...] We found that the distribution of deleterious variants in ACE2 differs among 9 populations in gnomAD (v3). Specifically, 39% (24/61) and 54% (33/61) of deleterious variants in ACE2 occur in African/African-American (AFR) and Non-Finnish European (EUR) populations, respectively (Fig. 1b). Prevalence of deleterious variants among Latino/Admixed American (AMR), East Asian (EAS), Finnish (FIN), and South Asian (SAS) populations is 2–10%, while Amish (AMI) and Ashkenazi Jewish (ASJ) populations do not appear to carry such variants in ACE2 coding regions (Fig. 1b). Specifically, several variants, including p.Met383Thr, p.Pro389His, and p.Asp427Tyr, have been reported to slightly inhibit the interaction between ACE2 and the spike protein of SARS-CoV-1 [10], which caused the first global SARS-CoV-1 outbreak. [...]

[...]

Abstract:

We are currently witnessing a major epidemic caused by the 2019 novel coronavirus (2019- nCoV). The evolution of 2019-nCoV remains elusive. We found 4 insertions in the spike glycoprotein (S) which are unique to the 2019-nCoV and are not present in other coronaviruses. Importantly, amino acid residues in all the 4 inserts have identity or similarity to those in the HIV-1 gp120 or HIV-1 Gag. Interestingly, despite the inserts being discontinuous on the primary amino acid sequence, 3D-modelling of the 2019-nCoV suggests that they converge to constitute the receptor binding site. The finding of 4 unique inserts in the 2019-nCoV, all of which have identity /similarity to amino acid residues in key structural proteins of HIV-1 is unlikely to be fortuitous in nature. This work provides yet unknown insights on 2019-nCoV and sheds light on the evolution and pathogenicity of this virus with important implications for diagnosis of this virus.

[...]

LONDON, Feb 1 (Reuters) - Leading South African scientists are set to investigate COVID-19 and HIV in tandem, amid mounting evidence that the collision of the two pandemics could be generating new coronavirus variants.

Abstract

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the agent of a major global outbreak of respiratory tract disease known as coronavirus disease-2019 (COVID-19). SARS-CoV-2 infects mainly lungs and may cause several immune-related complications, such as lymphocytopenia and cytokine storm, which are associated with the severity of the disease and predict mortality^1,2. The mechanism by which SARS-CoV-2 infection may result in immune system dysfunction is still not fully understood. Here we show that SARS-CoV-2 infects human CD4⁺ T helper cells, but not CD8⁺ T cells, and is present in blood and bronchoalveolar lavage T helper cells of severe COVID-19 patients. We demonstrated that SARS-CoV-2 spike glycoprotein (S) directly binds to the CD4 molecule, which in turn mediates the entry of SARS-CoV-2 in T helper cells. This leads to impaired CD4 T cell function and may cause cell death. SARS-CoV-2-infected T helper cells express higher levels of IL-10, which is associated with viral persistence and disease severity. Thus, CD4-mediated SARS-CoV-2 infection of T helper cells may contribute to a poor immune response in COVID-19 patients.

Coronavirus disease 2019 (COVID-19) has rapidly spread across the globe^3,4, being declared a pandemic by the World Health Organization (WHO) on March 11^th, 2020. COVID-19 has caused millions of deaths around the world. Most of the deaths are associated with acute pneumonia, cardiovascular complications, and organ failure due to hypoxia, exacerbated inflammatory responses and widespread cell death^1,5. Individuals that progress to the severe stages of COVID-19 manifest marked alterations in the immune response, characterized by reduced overall protein synthesis, cytokine storm, lymphocytopenia and T cell exhaustion^6–8. In addition to these acute effects on the immune system, a considerable proportion of infected individuals present low titers of neutralizing antibodies^9,10. Moreover, the levels of antibodies against SARS-CoV-2 decay rapidly after recovery in part of the infected individuals¹¹, suggesting that SARS-CoV-2 infection may exert profound and long-lasting complications to adaptive immunity. Recently, it has been shown that SARS-CoV-2 is able to infect lymphocytes^12,13. In this context, it is urgent to characterize the replicative capacity and the effects of SARS-CoV-2 replication in different immune cells, especially those involved with the formation of immunological memory and effective adaptive response, such as CD4⁺ T lymphocytes.

In what has been proposed to be the canonical mechanism of SARS-CoV-2 infection, the spike glycoprotein of SARS-CoV-2 (sCoV-2) binds to the host angiotensin-converting enzyme 2 (ACE2), after which it is cleaved by TMPRSS2¹⁴. While TMPRSS2 is ubiquitously expressed in human tissues (Extended Data Fig. 1), ACE2 is mainly expressed in epithelial and endothelial cells, as well as in the kidney, testis and small intestine (Extended Data Fig.1). Still, a wide variety of cell types are potentially infected by SARS-CoV-2^15–18, even though some of these cells express very low levels of ACE2. We showed this is the case for lymphocytes (Extended Data Fig. 2). These findings suggest that either SARS-CoV-2 uses alternative mechanisms to enter these cells or that auxiliary molecules at the plasma membrane may promote infection by stabilizing the virus until it interacts with ACE2. In agreement with the latter, binding of sCoV-2 to certain cell surface proteins facilitates viral entry^19,20.

[...]

Since the structures of the spike of SARS-CoV-1 (sCoV-1) and the sCoV-2 proteins are similar^21,22, we used the P-HIPSTer algorithm to uncover human proteins that putatively interact with spike²³. Seventy-one human proteins were predicted to interact with sCoV-1 (Extended Data Fig. 3). We then cross-referenced the proteins with five databases of plasma membrane proteins to identify the ones located on the cell surface (see Methods for details). CD4 was the only protein predicted to interact with sCoV-1 that appeared in all five databases (Extended Data Fig.3). CD4 is expressed mainly in T helper lymphocytes and has been shown to be the co-receptor to HIV²⁴. Since CD4⁺ T lymphocytes orchestrate innate and adaptive immune response^25,26, infection of CD4⁺ T cells by SARS-CoV-2 could explain lymphocytopenia and dysregulated inflammatory response in severe COVID-19 patients. Moreover, from an evolutionary perspective, infection of CD4⁺ T cells represents an effective mechanism for viruses to escape the immune response²⁷.

[...]

? The puzzle pieces continue to fall into place, and a significant new puzzle piece dropped last week, in the form of a preprint published to MedRxIV on July 31st, titled “SARS-CoV-2 Uses CD4 to Infect T Helper Lymphocytes.”

Although “just” a preprint, it features no fewer than seventy-seven authors. And it has already gathered three positive peer reviews. Let’s start with their conclusion, and then try to unpack what it means. The study’s admittedly obscure conclusion:

We demonstrated that SARS-CoV-2 spike glycoprotein (S) directly binds to the CD4 molecule, which in turn mediates the entry of SARS-CoV-2 in T helper cells. This leads to impaired CD4 T cell function and may cause cell death. SARS-CoV-2-infected T helper cells express higher levels of IL-10, which is associated with viral persistence and disease severity. Thus, CD4-mediated SARS-CoV-2 infection of T helper cells may contribute to a poor immune response in COVID-19 patients.

The researchers figured this out by first using sophisticated genetic software to analyze covid’s RNA. The results showed that covid’s spike protein potentially interacts with 77 different human tissues. But, after they filtered the results for proteins found on the outside of human cells, which are accessible to the spike, they found only one match: something called CD4 helper cells.

Then the researchers proved that covid does target CD4 cells in vivo, including by infecting previously un-infected blood, and by testing blood samples from recovering covid patients. They were very careful and the result seems pretty well established. So it almost seems like the spike was designed to attack this one particular type of cell. But what is it?

CD4 cells are also called “T helper cells.” They are a type of white blood cell playing a critical role in the immune system. Specifically, CD4 is a key part of the adaptive immune response, which is the body's initial defense mechanism against infections.

In fact, at bottom your immune system is coordinated by CD4 cells, which are the front line of recognizing invasive pathogens like viruses and bacteria. The CD4 cells raise an alarm, prompting other types of immune cells to respond appropriately. CD4 accomplishes this by releasing ‘signaling molecules’ called cytokines. In turn, cytokines regulate the activity of more complex immune cells.

Not to beat a dead horse, but CD4 cells are especially important in coordinating the immune response against infections, and they are central to the body's ability to remember and respond to specific pathogens. However, certain viruses, like HIV, specifically target and infect CD4 cells themselves, thereby knocking out the frontline immune response and weakening the overall immune system — which alarmingly creates increased vulnerability to other opportunistic infections.

Opportunistic infections like monkeypox, Hansen’s disease, RSV, and so on. Just to name a few, at random.

So what does all this mean, beyond a weakened immune system? The researchers speculated:

Infection of CD4+ T cells by SARS-CoV-2 could explain lymphocytopenia and dysregulated inflammatory response in severe COVID-19 patients. Moreover, from an evolutionary perspective, infection of CD4+ T cells represents an effective mechanism for viruses to escape the immune response.

In other words, the spike protein’s CD4-attacking feature seems almost designed to avoid the human immune response. Just what you’d want in a bioweapon, for example.

Once inside the CD4 cell, the covid virus weakens and kills it, destroying part of the immune system each time it happens. Worse, this process increases systemic levels of an inflammatory cytokine called Interleukin-10 (IL-10 ), which is associated with “viral persistence,” meaning an IL-10 inflammation makes it harder for the body to clear an infection. So covid — specifically its spike protein — hits the immune system two different ways.

Ultimately, the authors conceded that we don’t know how long the effect lasts:

How long these alterations in T cell function persist in vivo and whether they have long-lasting impacts on adaptive immunity remains to be determined.

But we do know one thing. Every time someone takes a jab, they reset their doses of spike, flooding their bodies with another few months worth. Back at the time the FDA “approved” the safest and most effective vaccines in human history, this effect of attacking the immune system through CD4 was unknown. One wonders, doesn’t one, whether it would have made any difference had these dangerous knock-on effects been publicly known.

Anyway, and most significantly, the authors ended by proposing further research to help develop clinical treatments based on knowing about covid’s CD4-targeted behavior:

Hence, avoiding T cell infection by blocking SARS-CoV-2—CD4 interaction and boosting T cell resistance against SARS-CoV-2 might represent complementary therapeutic approaches to preserve immune response integrity and prevent patients from progressing to the severe stages of COVID-19.

In other words — millions of lives might have been saved had we had known about this problem early in the pandemic. But instead, all those people were given useless remdesivir treatments and smothered by ventilators. And they died in large numbers.

Now let’s take a look at the indisputable evidence that damns the United States government, especially its bloated health agencies.

? Guess what the evidence shows? Fauci and the NIH knew all along. On January 30th of 2020 — right at the start of the pandemic — a group of Indian researchers published a study, which was nearly immediately forced to be withdrawn, that claimed HIV genes were found inserted into covid’s RNA. HIV also targets the CD4 cell.

So the problem wasn’t hard to find. But even if the CDC and the NIH somehow never saw the withdrawn study, a FOIA’d email dated Tuesday, February 4th, 2020, proves that reprehensible human cockroach Anthony Fauci was separately and directly told about this immuno-destructive feature of covid, at the time when the knowledge could have saved countless lives, but he arrogantly dismissed it. (Or worse, he and the NIH actively suppressed the information.)

Here’s the proof:

There was no good reason for the NIH to fail to follow up on this email. Even bypassing Fauci’s dismissive tone, a tone — “this person” — suggesting the emailer should be submerged in the nearest septic tank until he stopped kicking, even overlooking all that: Fauci forwarded the email to NIH staff for action.

But nothing happened. It just went away.

Remember: as the new study suggested, we might have developed treatments to deal with CD4 infection and IL-10 cytokine expression, treatments that would have saved countless lives. Instead, what did the NIH do? Nothing. Or worse, they aggressively suppressed the discovery.

Maybe they suppressed it because of Fauci’s long, sordid history with HIV. Fauci needed another HIV scandal like a hole in the cranium.

Think about it. Even setting aside the panoply of conspiracy facts suggesting much darker motives, in early February of 2020 Fauci was looking at a brand-new (“novel”) coronavirus to play with. He probably knew full well that thousands of germaphobes would soon be 3D-printing idolic Fauci bobbleheads and setting up little Fauci shrines. The last thing Fauci wanted would’ve been to drag all that old HIV baggage into the covid pandemic.

If that happened, everybody would just be remembering how the bureaucratic human barnacle bungled the HIV pandemic.

And who knows? They might have even pulled him off the project, because of the awful optics. Worse, maybe that ridiculous buffoon Luc Montagnier might’ve been put in charge of the response. Montagnier’s Nobel prize for HIV should’ve been Fauci’s, if it weren’t for all those meddling gay Americans who muddled the waters so much.

But that’s not all. Not even close.

? Let’s not forget about the money. This clip compilation by pandemic heroine Texas Lindsay (may God bless her and keep her long upon the Earth) is relevant and mind-blowing. You might want to watch it twice. Lindsay’s five-minute clip assembled the entire story, but please don’t miss Fauci’s appearance expressing his 2019 desire, his “hope,” to “rapidly respond to something brand new.”

Here’s the point. Forget about ivermectin and hydroxychloroquine for a minute. If an effective treatment targeting covid’s deadliest unique mechanism of harm had been developed, a treatment that could have interrupted the destructive autoimmune cytokine storm by, say, blocking covid’s attack on CD4 cells, the entire pandemic would have been avoided.

And if that had happened, if the pandemic had been avoided, mass mail-in ballots wouldn’t have been authorized, Trump would have been re-elected, the NIH would never have earned billions, and millions of costly social security recipients would still be alive. Not to mention the losses to all the downstream pandemic beneficiaries like Amazon, Bill Gates, corporate media, social media, hospitals, military bio-contractors, and local governments that would never had gotten paid.

To a large group of amoral, devil-worshipping, government-enriched élites, that would have been a catastrophe.

? But it may even be worse than that. If, as the study suggests, covid includes HIV, and works like HIV, then it is possible that the worst is yet to come. HIV starts with cold-like symptoms, just like covid, but then remains dormant for 8-10 years before the truly serious immune deterioration begins.

The connections between covid and HIV aren’t new. Over the last two years, there have been any number of signs of similarities cropping up between HIV and covid, as well as increasing government interest in HIV. For just one example, you’ll recall last year’s push for everyone to get tested for HIV:

Or this headline from the Hill in January 2022:

[...]

? Now remember: we’ve proven Fauci and the NIH knew about covid’s HIV-like effects in February 2020. Yet they rabidly censored all discussion about the problem, even to the extent of shutting down all research or even speculation into the bioweapons design of the virus. After all, if covid was zoonotic (naturally evolved in bats) nobody would even consider something like this. In other words, don’t be silly, what do bats have to do with HIV?

Here’s the bottom line. The decision to include spike protein in the experimental shots may wind up being the most deadly, recklessly negligent, reprehensible, and ultimately horrifying decision ever to emerge from fevered imaginations of mediocre government scientists. Spike’s mechanism of attacking CD4 cells — directly attacking the immune system itself — should have been an absolute disqualifier for inclusion of spike protein in the jabs.

[...]

Abstract

Novel coronavirus disease 2019 (COVID-19) is the biggest threat to human being globally. The first case was identified in a patient with flu symptoms along with severe acute respiratory syndrome in Wuhan, China in December 2019 and now it has spread in more than 200 countries. COVID-19 is more lethal in the elderly and people with an underlying condition such as asthma, cancer, diabetes. Here we performed bioinformatic analysis to investigate the interaction of S2 subunit protein of SARS-nCoV-2 of novel coronavirus with tumor suppressor proteins p53 and BRCA-1/2. In this short communication we report the interaction between S2 subunit proteins with tumor suppressor proteins for the first time. This preliminary result will open up a new direction to investigate the effect of a novel coronavirus in cancer patients.

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and COVID-19 infection has led to worsened outcomes for patients with cancer. SARS-CoV-2 spike protein mediates host cell infection and cell-cell fusion that causes stabilization of tumor suppressor p53 protein. In-silico analysis previously suggested that SARS-CoV-2 spike interacts with p53 directly but this putative interaction has not been demonstrated in cells. We examined the interaction between SARS-CoV-2 spike, p53 and MDM2 (E3 ligase, which mediates p53 degradation) in cancer cells using an immunoprecipitation assay. We observed that SARS-CoV-2 spike protein interrupts p53-MDM2 protein interaction but did not detect SARS-CoV-2 spike bound with p53 protein in the cancer cells. We further observed that SARS-CoV-2 spike suppresses p53 transcriptional activity in cancer cells including after nutlin exposure of wild-type p53-, spike S2-expressing tumor cells and inhibits chemotherapy-induced p53 gene activation of p21(WAF1), TRAIL Death Receptor DR5 and MDM2. The suppressive effect of SARS-CoV-2 spike on p53-dependent gene activation provides a potential molecular mechanism by which SARS-CoV-2 infection may impact tumorigenesis, tumor progression and chemotherapy sensitivity. In fact, cisplatin-treated tumor cells expressing spike S2 were found to have increased cell viability as compared to control cells. Further observations on gamma-H2AX expression in spike S2-expressing cells treated with cisplatin may indicate altered DNA damage sensing in the DNA damage response pathway. The preliminary observations reported here warrant further studies to unravel the impact of SARS-CoV-2 and its various encoded proteins including spike on pathways of tumorigenesis and response to cancer therapeutics.

Abstract

The present review aims to help the scientific community to better understand, in vitro and in vivo, COVID-19 compared to Monge disease (MD). The SARS-COV-2 or Corona-nanoparticles (NPs: 60-140nm) model based on nanosciences give an innovative understanding of virus nanotoxicity associated with violent inflammatory reactions and acute respiratory distress. Our analysis of COVID-19 suggests for the first time as far as we know that SARS-COV-2 use nanosciences laws such as virus agglomeration and mitochondria respiration toxicity induced by cluster virus-Heme. Moreover, the implication of age, gender, and ethnicity to COVID-19 must be confirmed by future studies compared to MD. The virus could use nano mechanisms to induce hypoxia via the generation of Heme-virus clusters mitigating micro coagulation implicated in acute respiratory distress and heart failure. Our analysis points to the presence of a possible link between hypoxia and COVID-19 pro-pulmonary complications.

US Governement (NIAID) sponsored studies specifically focused on Bat, "SARS-like" Coronavirus originations and designations. (link)

Ralph Baric, an infectious-disease researcher at the University of North Carolina at Chapel Hill, last week (November 9) published a study on his team’s efforts to engineer a virus with the surface protein of the SHC014 coronavirus, found in horseshoe bats in China, and the backbone of one that causes human-like severe acute respiratory syndrome (SARS) in mice. The hybrid virus could infect human airway cells and caused disease in mice, according to the team’s results, which were published in Nature Medicine. [ archived link ]

The results demonstrate the ability of the SHC014 surface protein to bind and infect human cells, validating concerns that this virus—or other coronaviruses found in bat species—may be capable of making the leap to people without first evolving in an intermediate host, Nature reported. They also reignite a debate about whether that information justifies the risk of such work, known as gain-of-function research. “If the [new] virus escaped, nobody could predict the trajectory,” Simon Wain-Hobson, a virologist at the Pasteur Institute in Paris, told Nature.

In October 2013, the US government put a stop to all federal funding for gain-of-function studies, with particular concern rising about influenza, SARS, and Middle East respiratory syndrome (MERS). “NIH [National Institutes of Health] has funded such studies because they help define the fundamental nature of human-pathogen interactions, enable the assessment of the pandemic potential of emerging infectious agents, and inform public health and preparedness efforts,” NIH Director Francis Collins said in a statement at the time. “These studies, however, also entail biosafety and biosecurity risks, which need to be understood better.”

Exclusive information. Multiple highly regarded scientists who have studied C0R0NAVlRUS say that the VlRUS has been manipulated in labs to better attach to human cells. Turns out, research on that very thing was conducted here in the United States until the research was banned in 2013. In 2014, the research appears to have resumed through funding to several labs in China through payments to Eco Health Alliance. We break down the timeline.

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COVID-19 – A Biological Weapon Targeting Ethnicity and Body Systems

Zhao was soon joined by bioweapons experts like Francis Boyle, prominent virologists Luc Montagnier and Judy Mikovits, followed by a growing array of scholars, scientists and academics from around the world who all assessed that the virus’ apparent gene sequencing implied human handiwork. While all agreed that COVID appeared to have originated from a lab, it was still unclear whether that lab was Chinese or controlled by the USA.

Another obvious question arose with this lab theory: Was it an accidental leak or was it consciously deployed?

Since pandemic war game operations had become a normalized part of western geopolitical life from the early days of Dark Winter in 2000 to the Rockefeller Foundation’s 2011 Lock Step to the World Economic Forum’s Event 201 (and dozens more in between), the likelihood of conscious deployment was a very serious possibility.

[...]

Stop the next pandemic before it starts.

[...]

There are 14 biosafety level 4 (BSL-4) labs in the United States.

If you count biosafety level 3 (BSL-3) labs, there are more than 200! And, that’s from a USA Today investigation back in 2015! Even more high-containment labs are operating now.

Is there one in your backyard?

If you’re in Maryland near Washington, DC, like I am, you’re in the belly of the biolab beast where three BSL-4 and thirteen BSL-3 labs are in operation! We’ve already got a protest going every Wednesday at noon against Anthony Fauci, who runs several BSL-4 labs, including the NIAID Integrated Research Facility at Fort Detrick where the anthrax used in the 2001 false flag attacks is said to have originated. Three of the people involved in Amerithrax are key players in COVID-19. Former Fort Detrick commander David Franz who had a DARPA contract to create the attack anthrax now works for EcoHealth Alliance, the US partner and funder of the Wuhan Institute of Virology. Trump’s Assistant Secretary for Preparedness and Response Robert Kadlec helped Emergent Biosolutions profit off the 2001 attacks and COVID-19. Kadlec’s deputy, ​​David Christian “Chris” Hassell was the FBI lab director who pinned the anthrax attacks on patsy Bruce Ivins. Hassell now serves as the only known member of the secret committee funding gain-of-function research.

[...]

Key Messages:

• Within 4 weeks following infection, 90-99% of individuals infected with the SARS-CoV-2 virus develop detectable neutralizing antibodies.
• The strength and duration of the immune responses to SARS-CoV-2 are not completely understood and currently available data suggests that it varies by age and the severity of symptoms. Available scientific data suggests that in most people immune responses remain robust and protective against reinfection for at least 6-8 months after infection (the longest follow up with strong scientific evidence is currently approximately 8 months).
• Some variant SARS-CoV-2 viruses with key changes in the spike protein have a reduced susceptibility to neutralization by antibodies in the blood. While neutralizing antibodies mainly target the spike protein, cellular immunity elicited by natural infection also target other viral proteins, which tend to be more conserved across variants than the spike protein. The ability of emerging virus variants (variants of interest and variants of concern) to evade immune responses is under investigation by researchers around the world.
• There are many available serologic assays that measure the antibody response to SARS-CoV-2 infection, but at the present time, the correlates of protection are not well understood

Generating immunity against the SARS-CoV-2 coronavirus is of the utmost importance for bringing the COVID-19 pandemic under control, protecting vulnerable individuals from severe disease and limiting viral spread. Our immune systems protect against SARS-CoV-2 either through a sophisticated reaction to infection or in response to vaccination. A key question is, how long does this immunity last? Writing in Nature, Turner et al.¹ and Wang et al.² characterize human immune responses to SARS-CoV-2 infection over the course of a year.

There is ongoing discussion about which aspects of the immune response to SARS-CoV-2 provide hallmarks of immunity (in other words, correlates of immunological protection). However, there is probably a consensus that the two main pillars of an antiviral response are immune cells called cytotoxic T cells, which can selectively eliminate infected cells, and neutralizing antibodies, a type of antibody that prevents a virus from infecting cells, and that is secreted by immune cells called plasma cells. A third pillar of an effective immune response would be the generation of T helper cells, which are specific for the virus and coordinate the immune reaction. Crucially, these latter cells are required for generating immunological memory — in particular, for orchestrating the emergence of long-lived plasma cells³, which continue to secrete antiviral antibodies even when the virus has gone.

[...]

The levels of IgG antibodies against SARS-CoV-2 Spike protein remain stable, or even increase, seven months after infection, according to a follow-up study in a cohort of healthcare workers coordinated by the Barcelona Institute for Global Health (ISGlobal), an institution supported by “la Caixa” Foundation, in collaboration with the Hospital Clinic of Barcelona. The results, published in Nature Communications, also support the idea that pre-existing antibodies against common cold coronaviruses could protect against COVID-19.

[...]

Highlights

• Most recovered COVID-19 patients mount broad, durable immunity after infection
• Neutralizing antibodies show a bi-phasic decay with half-lives >200 days
• Spike IgG+ memory B cells increase and persist postinfection
• Durable polyfunctional CD4 and CD8 T cells recognize distinct viral epitope regions

Findings

We report broad serological profiles within the cohort, detecting antibody binding to other human coronaviruses. 202(>99%) participants had SARS-CoV-2 specific antibodies, with SARS-CoV-2 neutralization and spike-ACE2 receptor interaction blocking observed in 193(95%) individuals. A significant positive correlation (r=0.7804) between spike-ACE2 blocking antibody titers and neutralization potency was observed. Further, SARS-CoV-2 specific CD8 T-cell responses were clear and quantifiable in 95 of 106(90%) HLA-A2 individuals.

Interpretation

• The immune systems of more than 95% of people who recovered from COVID-19 had durable memories of the virus up to eight months after infection.
• The results provide hope that people receiving SARS-CoV-2 vaccines will develop similar lasting immune memories after vaccination.

Conclusions

It is unclear why NSP7- and NSP13-specific T cells are detected and often dominant in unexposed donors, while representing a minor population in individuals who have recovered from SARS or COVID-19. It is, however, consistent with the findings of a previous study, in which ORF1-specific T cells were preferentially detected in some donors who were not exposed to SARS-CoV-2 whereas T cells from individuals who had recovered from COVID-19 preferentially recognized structural proteins. Induction of virus-specific T cells in individuals who were exposed but uninfected has been demonstrated in other viral infections. Theoretically, individuals exposed to coronaviruses might just prime ORF1-specific T cells, as the ORF1-encoded proteins are produced first in coronavirus-infected cells and are necessary for the formation of the viral replicase–transcriptase complex that is essential for the subsequent transcription of the viral genome, which then leads to the expression of various RNA species. Therefore, ORF1-specific T cells could hypothetically abort viral production by lysing SARS-CoV-2-infected cells before the formation of mature virions. By contrast, in patients with COVID-19 and SARS, the N protein—which is abundantly produced in cells that secrete mature virions—would be expected to preferentially boost N-specific T cells.

Notably, the ORF1 region contains domains that are highly conserved among many different coronaviruses. The distribution of these viruses in different animal species might result in periodic human contact that induces ORF1-specific T cells with cross-reactive abilities against SARS-CoV-2. Understanding the distribution, frequency and protective capacity of pre-existing structural or non-structural protein-associated SARS-CoV-2 cross-reactive T cells could be important for the explanation of some of the differences in infection rates or pathology observed during this pandemic. T cells that are specific to viral proteins are protective in animal models of airway infections, but the possible effects of pre-existing N- and/or ORF1-specific T cells onthe differential modulation of SARS-CoV-2 infection will have to be carefully evaluated.

CONCLUSION

Our study demonstrates that convalescent subjects previously infected with ancestral variant SARS-CoV-2 produce antibodies that cross-neutralize emerging VOCs with high potency. Structural and functional analyses reveal that antibody breadth is mediated by targeting a site of vulnerability at the RBD tip offset from major mutational hotspots in VOCs. Selective boosting of immune responses targeting specific RBD epitopes, such as the sites defined by these antibodies, may induce breadth against current and future VOCs.

[...]

We reviewed studies published in PubMed from inception to Sept 28, 2021, and found well conducted biological studies showing protective immunity after infection (panel). Furthermore, multiple epidemiological and clinical studies, including studies during the recent period of predominantly delta (B.1.617.2) variant transmission, found that the risk of repeat SARS-CoV-2 infection decreased by 80·5–100% among those who had had COVID-19 previously (panel). The reported studies were large and conducted throughout the world. Another laboratory-based study that analysed the test results of 9119 people with previous COVID-19 from Dec 1, 2019, to Nov 13, 2020, found that only 0·7% became reinfected.¹¹ In a study conducted at the Cleveland Clinic in Cleveland, OH, USA, those who had not previously been infected had a COVID-19 incidence rate of 4·3 per 100 people, whereas those who had previously been infected had a COVID-19 incidence rate of 0 per 100 people.⁶ Furthermore, a study conducted in Austria found that the frequency of hospitalisation due to a repeated infection was five per 14 840 (0·03%) people and the frequency of death due to a repeated infection was one per 14 840 (0·01%) people.⁴ Due to the strong association and biological basis for protection,¹² clinicians should consider counselling recovered patients on their risk for reinfection and document previous infection status in medical records.

[...]

We should not force COVID vaccines on anyone when the evidence shows that naturally acquired immunity is equal to or more robust and superior to existing vaccines. Instead, we should respect the right of the bodily integrity of individuals to decide for themselves. 

Public health officials and the medical establishment with the help of the politicized media are misleading the public with assertions that the COVID-19 shots provide greater protection than natural immunity. CDC Director Rochelle Walensky, for example, was deceptive in her October 2020 published LANCET statement that “there is no evidence for lasting protective immunity to SARS-CoV-2 following natural infection” and that “the consequence of waning immunity would present a risk to vulnerable populations for the indefinite future.” 

Immunology and virology 101 have taught us over a century that natural immunity confers protection against a respiratory virus’s outer coat proteins, and not just one, e.g. the SARS-CoV-2 spike glycoprotein. There is even strong evidence for the persistence of antibodies. Even the CDC recognizes natural immunity for chicken-pox and measles, mumps, and rubella, but not for COVID-19. 

[...]

[...]

In many countries natural immunity is recognized, at least in some part, as a valid reason to refrain from a COVID vaccine. Here in the U.S., many people facing mandates are unable to use their natural immunity as a justified reason to pass on the vaccine. In fact, it’s almost as if we’d never encountered natural immunity before. Which is odd considering vaccines are developed to mimic the natural immune response.

Several studies, as well as the CDC and other governmental agencies around the world, have come out to say that the immune response induced by the COVID vaccines wanes rather quickly. This is the justification and reason that warrants the need for boosters after just 6 months.

Those who choose to argue that natural immunity may not be suitable, argue that we don’t have long term studies. In fact, we have several studies. Well done studies that indicate that natural immunity is not only robust, but also far superior to the vaccine-induced immune response. So far, as we see vaccine-induced immune responses waning, we’ve yet to see one where natural immunity wanes nearly as quickly.

As concerns continue to mount for ADE, myocarditis, Guillain-Barre Syndrome, blood clots, nervous system disorders and a whole host of other conditions in the growing number of VAERS reports, elicited by the vaccines, we need to take a serious look at natural immunity.

While we wait for long-term studies on the vaccines to be conducted and reported on, we have these at our fingertips. If the FDA continues to push for 55, and now doubled-down for 75 years to release the data that led them to an EUA approval, we can use this information in the meantime to make an informed decision.

[...]

Natural immunity will be key to downshifting the pandemic to endemic status. That doesn’t mean you should go out and try to catch the virus tomorrow.

In October 2020, a few weeks before the experimental trial results for the BioNTech-Pfizer, Moderna and Oxford/AstraZeneca Covid-19 vaccines were released, German virologist Christian Drosten cautioned that the shots would be of limited effectiveness in preventing the spread of the disease.

“We are dealing here with an infection of the mucous membrane, i.e., in the nose and the throat and then later the lungs,” he said on Episode 62 of Das Coronavirus-Update, the podcast launched by broadcaster NDR in March 2020 that helped make Drosten a household name in Germany. “The mucous membranes already have their own special local immune system. With the current vaccines, which are more likely to be injected into the muscle, you don’t reach this local immune system so well.” As a result, the vaccines “probably protect more against the severe course [of the disease] than against infection.”

Which is of course exactly how things played out. The vaccines have been spectacularly effective at preventing severe disease and death, much less so at preventing transmission.

Drosten has been described in the U.S. media as “Germany’s Fauci,” but the moniker seems a little unfair. National Institute of Allergy and Infectious Diseases Director Anthony Fauci was a top researcher in his day, but has been running a sizable government agency (fiscal year 2021 budget, $6 billion) for the past 38 years. His appearances in the media during the pandemic have mostly involved reciting the public-health consensus of the moment, which was useful when the U.S. president was a font of Covid-19 misinformation but not always especially enlightening. Drosten, director of the Institute of Virology at Berlin’s Charité medical school, is perhaps the world’s leading coronavirus expert, responsible for identifying the original severe acute respiratory syndrome virus in 2003 and devising the first diagnostic test for the Covid-causing SARS-CoV-2 virus in January 2020. His public commentary, delivered chiefly in podcast form after he grew frustrated dealing with some in the German media, has tended toward the cutting-edge and forward-looking — as indicated by what he was saying about vaccines in October 2020.

I recount all this as context for what Drosten said last month in the 113th and final (for now) regular Coronavirus-Update episode. He was talking again about the mucous membrane — which in German is conveyed as the more graphic “Schleimhaut,” literally “slime skin” — and its role in keeping infectious diseases in check (translation and editing-for-brevity by me):

With influenza it is simply the case that everyone gets infected x times over the course of their lives. These infections occur in the mucous membrane, in the throat. Our mucous membranes have a local immune system of their own, if you want to call it that. And everyone in the population, except for the children, of course, has so many infections behind them that there in the mucous membrane, immunity exists. That is why the adults in the population, and that is the vast majority of the population, are not so infectious.

[...]

[...]

Even I knew (from what I learned in 9th grade and what my mother taught) that the pandemic would only end with endemicity naturally earned. That is precisely what is happening. The CDC’s publication MMWR printed a seroprevalence study showing that from December 2021 to February 2022 – that period during which it seemed like everyone in the country got covid – went from 33.5% to 57.7%. In children, it went from 44.2% to 75.2%. It’s higher in both groups now. 

That the study got no real attention to it shows that we are fast moving toward the end, and how? Not through vaccination, which protects against neither infection nor transmission. It ends with everyone meeting the virus. There is of course some threshold of herd immunity with this virus, though it keeps rising with each mutation, requiring ever more rounds of infection to achieve it. It is surely higher than 70% but probably less than 90% depending on population mobility and other factors. 

We can look at that data today and wonder. What if we had never locked down? What if we had gone on with life as normally while urging those in risk categories to wait it out a bit while we achieved endemicity? How long would it have taken to get there? 

Might it have been over by the summer of 2020? It is possible. It’s hard to know such counterfactuals with precision, but it does seem highly likely that the lockdowns achieved nothing good, caused tremendous damage, and also unnecessarily prolonged the pandemic. In addition, they degraded everyone’s immune system: we didn’t just avoid covid but everything else too. 

And the main reason was due to the unwillingness of public health authorities to talk about actual science. When Fauci was asked about natural immunity in September 2021, he said “I don’t have a really firm answer for you on that. That’s something that we’re going to have to discuss regarding the durability of the response…I think that is something that we need to sit down and discuss seriously.”

The WHO even changed its definition of herd immunity to exclude natural infection as a factor! The whole institution gave itself over to vaccine sales based on wild exaggerations of their effectiveness while all-but-denying robust and broad immunity through exposure. 

[...]

Abstract

BACKGROUND: The future of the SARS-CoV-2 pandemic hinges on virus evolution and duration of immune protection of natural infection against reinfection. We investigated duration of protection afforded by natural infection, the effect of viral immune evasion on duration of protection, and protection against severe reinfection, in Qatar, between February 28, 2020 and June 5, 2022. METHODS: Three national, matched, retrospective cohort studies were conducted to compare incidence of SARS-CoV-2 infection and COVID-19 severity among unvaccinated persons with a documented SARS-CoV-2 primary infection, to incidence among those infection-naive and unvaccinated. Associations were estimated using Cox proportional-hazard regression models. RESULTS: Effectiveness of pre-Omicron primary infection against pre-Omicron reinfection was 85.5% (95% CI: 84.8-86.2%). Effectiveness peaked at 90.5% (95% CI: 88.4-92.3%) in the 7th month after the primary infection, but waned to ~70% by the 16th month. Extrapolating this waning trend using a Gompertz curve suggested an effectiveness of 50% in the 22nd month and <10% by the 32nd month. Effectiveness of pre-Omicron primary infection against Omicron reinfection was 38.1% (95% CI: 36.3-39.8%) and declined with time since primary infection. A Gompertz curve suggested an effectiveness of <10% by the 15th month. Effectiveness of primary infection against severe, critical, or fatal COVID-19 reinfection was 97.3% (95% CI: 94.9-98.6%), irrespective of the variant of primary infection or reinfection, and with no evidence for waning. Similar results were found in sub-group analyses for those ≥50 years of age. CONCLUSIONS: Protection of natural infection against reinfection wanes and may diminish within a few years. Viral immune evasion accelerates this waning. Protection against severe reinfection remains very strong, with no evidence for waning, irrespective of variant, for over 14 months after primary infection.

Abstract

Objective: To evaluate dynamics of antibody levels following exposure to SARS-CoV-2 during 12 months in Dutch non-vaccinated hairdressers and hospitality staff.

Methods: In this prospective cohort study, blood samples were collected every three months for one year, and analyzed using a qualitative total antibody ELISA and a quantitative IgG antibody ELISA. Participants filled out questionnaires, providing information on demographics, health and work. Differences in antibody levels were evaluated using Mann-Whitney U and Wilcoxon Signed Rank tests. Beta coefficients (B) and 95% confidence intervals (95%CI) were calculated using linear regression.

Results: Ninety-five of 497 participants (19.1%) had ≥1 seropositive measurement before their last visit using the qualitative ELISA. Only 2.1% (2/95) seroreverted during follow-up. Of the 95 participants, 82 (86.3%) tested IgG seropositive in the quantitative ELISA too. IgG antibody levels significantly decreased in the first months (p<0.01), but remained detectable up to 12 months in all participants. Higher age (B, 10-years increment: 24.6, 95%CI: 5.7-43.5) and higher BMI (B, 5kg/m² increment: 40.0, 95%CI: 2.9-77.2) were significantly associated with a higher peak of antibody levels.

Conclusions: In this cohort, SARS-CoV-2 antibodies persisted for up to one year after initial seropositivity, suggesting long-term natural immunity.

Summary

Background

Understanding the level and characteristics of protection from past SARS-CoV-2 infection against subsequent re-infection, symptomatic COVID-19 disease, and severe disease is essential for predicting future potential disease burden, for designing policies that restrict travel or access to venues where there is a high risk of transmission, and for informing choices about when to receive vaccine doses. We aimed to systematically synthesise studies to estimate protection from past infection by variant, and where data allow, by time since infection.

Methods

In this systematic review and meta-analysis, we identified, reviewed, and extracted from the scientific literature retrospective and prospective cohort studies and test-negative case-control studies published from inception up to Sept 31, 2022, that estimated the reduction in risk of COVID-19 among individuals with a past SARS-CoV-2 infection in comparison to those without a previous infection. We meta-analysed the effectiveness of past infection by outcome (infection, symptomatic disease, and severe disease), variant, and time since infection. We ran a Bayesian meta-regression to estimate the pooled estimates of protection. Risk-of-bias assessment was evaluated using the National Institutes of Health quality-assessment tools. The systematic review was PRISMA compliant and was registered with PROSPERO (number CRD42022303850).

Findings

We identified a total of 65 studies from 19 different countries. Our meta-analyses showed that protection from past infection and any symptomatic disease was high for ancestral, alpha, beta, and delta variants, but was substantially lower for the omicron BA.1 variant. Pooled effectiveness against re-infection by the omicron BA.1 variant was 45·3% (95% uncertainty interval [UI] 17·3–76·1) and 44·0% (26·5–65·0) against omicron BA.1 symptomatic disease. Mean pooled effectiveness was greater than 78% against severe disease (hospitalisation and death) for all variants, including omicron BA.1. Protection from re-infection from ancestral, alpha, and delta variants declined over time but remained at 78·6% (49·8–93·6) at 40 weeks. Protection against re-infection by the omicron BA.1 variant declined more rapidly and was estimated at 36·1% (24·4–51·3) at 40 weeks. On the other hand, protection against severe disease remained high for all variants, with 90·2% (69·7–97·5) for ancestral, alpha, and delta variants, and 88·9% (84·7–90·9) for omicron BA.1 at 40 weeks.

Interpretation

Protection from past infection against re-infection from pre-omicron variants was very high and remained high even after 40 weeks. Protection was substantially lower for the omicron BA.1 variant and declined more rapidly over time than protection against previous variants. Protection from severe disease was high for all variants. The immunity conferred by past infection should be weighed alongside protection from vaccination when assessing future disease burden from COVID-19, providing guidance on when individuals should be vaccinated, and designing policies that mandate vaccination for workers or restrict access, on the basis of immune status, to settings where the risk of transmission is high, such as travel and high-occupancy indoor settings.

Abstract

It has long been hypothesized that attractiveness provides a cue to a target's health and immunocompetence. However, much of the research testing this hypothesis has relied on a small number of indirect proxies of immune function, and the results of this research have been mixed. Here, we build on this past research, examining the relationship between target attractiveness and (i) self-reported health, (ii) in vivo measures of inflammation and white blood cell count/composition, and (iii) in vitro tests of targets' immune function, including (c₁) leucocyte proliferation in response to immunological stimulants, (c₂) phagocytosis of Escherichia coli bioparticles, (c₃) NK cell-mediated lysis of target tumour cells, and (c₄) Staphylococcus aureus growth in isolated plasma. Results revealed multiple, sometimes sex-differentiated, relationships between targets' immune function and others’ perceptions of their attractiveness. Together, this work suggests complex, often sex-differentiated relationships between immune function, health, and attractiveness.

[...]

6. Conclusion

Researchers have long speculated that perceptions of attractiveness reflect preferences for traits historically linked to health and, ultimately, immune function (e.g. [6]). The results of the current research suggest that facial attractiveness may provide insights into one's immune function, particularly as it relates to one's ability to efficiently combat (primarily) bacterial threats. Additionally, for men, facial attractiveness may also provide cues to their ability to efficiently manage viral threats and neoplastic growth. Although future research is needed replicate these results, the current research suggests that a relationship between facial attractiveness and immune function is likely to exist.

[...]

[...]

1) COVID-19 Infections (Infections due to SARS-CoV-2)

a) Code only confirmed cases Code only a confirmed diagnosis of the 2019 novel coronavirus disease (COVID-19) as documented by the provider, documentation of a positive COVID-19 test result, or a presumptive positive COVID-19 test result. For a confirmed diagnosis, assign code U07.1, COVID-19. This is an exception to the hospital inpatient guideline Section II, H. In this context, “confirmation” does not require documentation of the type of test performed; the provider’s documentation that the individual has COVID-19 is sufficient.

Presumptive positive COVID-19 test results should be coded as confirmed. A presumptive positive test result means an individual has tested positive for the virus at a local or state level, but it has not yet been confirmed by the Centers for Disease Control and Prevention (CDC). CDC confirmation of local and state tests for COVID-19 is no longer required.

If the provider documents "suspected," "possible," "probable," or “inconclusive” COVID19, do not assign code U07.1. Assign a code(s) explaining the reason for encounter (such as fever) or Z20.828, Contact with and (suspected) exposure to other viral communicable diseases.

[...]

Dr. Andrew Kaufman gives a presentation on:

- The COVID-19 disease
- PCR testing process and its inability to identify a virus
- Naturally occurring exosomes, how they're induced and their relation to virus bodies
- Overview of some treatments

For anyone willing to look, there are so many facts that tell the true story, and it goes something like this:

Knowing what we know today about COVID-19’s Infection Fatality Rate, asymmetric impact by age and medical condition, non-transmissibility by asymptomatic people and in outdoor settings, near-zero fatality rate for children, and the basic understanding of viruses through Farr’s law, locking down society was a bone-headed policy decision so devastating to society that historians may judge it as the all-time worst decision ever made. Worse, as these clear facts have become available, many policy-makers haven’t shifted their positions, despite the fact that every hour under any stage of lockdown has a domino-effect of devastation to society. Meanwhile, the media—with a few notable exceptions—is oddly silent on all the good news. Luckily, an unexpected group of heroes across the political landscape—many of them doctors and scientists—have emerged to tell the truth, despite facing extreme criticism and censorship from an angry mob desperate to continue fighting an imaginary war.

Jay Bhattacharya, a professor of medicine, told The Telegraph's Planet Normal podcast, which you can listen to using the audio player above, that there have been "enormous collateral consequences" of keeping people inside and isolating them from their loved-ones during the Covid-19 pandemic.

The epidemiologist believes many scientists have clung onto the perceived effectiveness of lockdowns, and they "remain attached" to the idea despite the "failure of this strategy".

"I do think that future historians will look back on this and say this was the single biggest public health mistake, possibly of all history, in terms of the scope of the harm that it's caused," said Prof Bhattacharya.

• With some 2.6 billion people around the world in some kind of lockdown, we are conducting arguably the largest psychological experiment ever;
• This will result in a secondary epidemic of burnouts and stress-related absenteeism in the latter half of 2020;
• Taking action now can mitigate the toxic effects of COVID-19 lockdowns.

New Zealand entered a strict three-day national lockdown Tuesday after a single case of coronavirus was detected in Auckland, the first locally transmitted example in six months.

The last community outbreak in the South Pacific nation was in February and New Zealand has reported just 26 virus deaths nationally since the pandemic began.

Despite that virus-free stretch, Prime Minister Jacinda Ardern confirmed she would move to Alert Level Four on the presumption the Delta variant has been isolated, saying it was important for the country to “go hard and go early.”

Level Four means reducing contact between people to the bare, essential minimum with the closing of schools, offices and all businesses with only essential services remaining operational.

“As we’ve seen overseas, particularly in Sydney, unnecessary trips outdoors can spread the virus,” the former president of the International Union of Socialist Youth said. (see below)

New South Wales (NSW) Premier Gladys Berejiklian said on Monday that seven people had died of Covid-19 in the past 24 hours. It is the highest number of related deaths in the region since the pandemic started.

The Administration is taking aggressive actions and exercising regulatory flexibilities to help healthcare providers contain the spread of 2019 Novel Coronavirus Disease (COVID-19). CMS is empowered to take proactive steps through 1135 waivers as well as, where applicable, authority granted under section 1812(f) of the Social Security Act (the Act) and rapidly expand the Administration’s aggressive efforts against COVID-19. As a result, the following blanket waivers are in effect, with a retroactive effective date of March 1, 2020, through the end of the emergency declaration. For general information about waivers, see Attachment A to this document. These waivers DO NOT require a request to be sent to the 1135waiver@cms.hhs.gov mailbox or that notification be made to any of CMS’ regional offices.

Unless otherwise noted, these waivers will terminate at the end of the COVID-19 public health emergency (PHE).

[...]

INTRODUCTION:

Under President Trump’s leadership, the Centers for Medicare & Medicaid Services (CMS) has broadened access to Medicare telehealth services so that beneficiaries can receive a wider range of services from their doctors without having to travel to a healthcare facility. These policy changes build on the regulatory flexibilities granted under the President’s emergency declaration. CMS is expanding this benefit on a temporary and emergency basis under the 1135 waiver authority and Coronavirus Preparedness and Response Supplemental Appropriations Act. The benefits are part of the broader effort by CMS and the White House Task Force to ensure that all Americans – particularly those at high-risk of complications from the virus that causes the disease COVID-19 – are aware of easy-to-use, accessible benefits that can help keep them healthy while helping to contain the community spread of this virus.

[...]

MEDICARE TELEHEALTH VISITS: Currently, Medicare patients may use telecommunication technology for office, hospital visits and other services that generally occur in-person. 

• The provider must use an interactive audio and video telecommunications system that permits real-time communication between the distant site and the patient at home. Distant site practitioners who can furnish and get payment for covered telehealth services (subject to state law) can include physicians, nurse practitioners, physician assistants, nurse midwives, certified nurse anesthetists, clinical psychologists, clinical social workers, registered dietitians, and nutrition professionals. 
• It is imperative during this public health emergency that patients avoid travel, when possible, to physicians’ offices, clinics, hospitals, or other health care facilities where they could risk their own or others’ exposure to further illness. Accordingly, the Department of Health and Human Services (HHS) is announcing a policy of enforcement discretion for Medicare telehealth services furnished pursuant to the waiver under section 1135(b)(8) of the Act. To the extent the waiver (section 1135(g)(3)) requires that the patient have a prior established relationship with a particular practitioner, HHS will not conduct audits to ensure that such a prior relationship existed for claims submitted during this public health emergency.

[...]

An exclusive group of thought leaders gathered at the museum to discuss how the world prepares for the next global pandemic, raises public awareness, and explores potential responses and solutions

Event 201 was a 3.5-hour pandemic tabletop exercise that simulated a series of dramatic, scenario-based facilitated discussions, confronting difficult, true-to-life dilemmas associated with response to a hypothetical, but scientifically plausible, pandemic. 15 global business, government, and public health leaders were players in the simulation exercise that highlighted unresolved real-world policy and economic issues that could be solved with sufficient political will, financial investment, and attention now and in the future.

The exercise consisted of pre-recorded news broadcasts, live “staff” briefings, and moderated discussions on specific topics. These issues were carefully designed in a compelling narrative that educated the participants and the audience.

The Johns Hopkins Center for Health Security, World Economic Forum, and Bill & Melinda Gates Foundation jointly propose these recommendations.

[...]

    This Act may be cited as the ``Coronavirus Aid, Relief, and Economic 
Security Act'' or the ``CARES Act''.

[...]

TITLE V--CORONAVIRUS RELIEF FUNDS

Sec. 5001. Coronavirus Relief Fund.

                   TITLE VI--MISCELLANEOUS PROVISIONS

Sec. 6001. COVID-19 borrowing authority for the United States Postal 
           Service.
Sec. 6002. Emergency designation.

DIVISION B--EMERGENCY APPROPRIATIONS FOR CORONAVIRUS HEALTH RESPONSE AND 
                            AGENCY OPERATIONS

[...]

WASHINGTON -- Nearly 1.1 million coronavirus relief payments totaling some $1.4 billion went to dead people, a government watchdog reported Thursday. Legal and political issues hang over the misdirected taxpayer funds, the latest example of errors in massive aid being dispensed at crisis speed.

More than 130 million so-called economic impact payments were sent to taxpayers as part of the $2.4 trillion coronavirus relief package enacted in March. The Government Accountability Office, Congress' auditing arm, cited the number of erroneous payments to deceased taxpayers in its report on the government programs.

[...]

TITLE III—GENERAL POWERS AND DUTIES OF PUBLIC HEALTH SERVICE

DATA COLLECTION REGARDING PROGRAMS UNDER TITLE XXVI SEC.

318B. ø247c–2¿ For the purpose of collecting and providing data for program planning and evaluation activities under title XXVI, there are authorized to be appropriated to the Secretary (acting through the Director of the Centers for Disease Control and Prevention) such sums as may be necessary for each of the fiscal years 2001 through 2005. Such authorization of appropriations is in addition to other authorizations of appropriations that are available for such purpose.

SEC. 319. ø247d¿ PUBLIC HEALTH EMERGENCIES.

(a) EMERGENCIES.—If the Secretary determines, after consultation with such public health officials as may be necessary, that— (1) a disease or disorder presents a public health emergency; or (2) a public health emergency, including significant outbreaks of infectious diseases or bioterrorist attacks, otherwise exists, the Secretary may take such action as may be appropriate to respond to the public health emergency, including making grants, providing awards for expenses, and entering into contracts and conducting and supporting investigations into the cause, treatment, or prevention of a disease or disorder as described in paragraphs (1) and (2). Any such determination of a public health emergency terminates upon the Secretary declaring that the emergency no longer exists, or upon the expiration of the 90-day period beginning on the date on which the determination is made by the Secretary, whichever occurs first. Determinations that terminate under the preceding sentence may be renewed by the Secretary (on the basis of the same or additional facts), and the preceding sentence applies to each such renewal. Not later than 48 hours after making a determination under this subsection of a public health emergency (including a renewal), the Secretary shall submit to the Congress written notification of the determination.

(b) PUBLIC HEALTH EMERGENCY FUND.—

(1) IN GENERAL.—There is established in the Treasury a fund to be designated as the ‘‘Public Health Emergency Fund’’ to be made available to the Secretary without fiscal year limitation to carry out subsection (a) only if a public health emergency has been declared by the Secretary under such subsection or if the Secretary determines there is the significant potential for a public health emergency, to allow the Secretary to rapidly respond to the immediate needs resulting from such public health emergency or potential public health emergency. The Secretary shall plan for the expedited distribution of funds to appropriate agencies and entities. There is authorized to be appropriated to the Fund such sums as may be necessary. (2) USES.—The Secretary may use amounts in the Fund established under paragraph (1), to— 

[...]

(C) facilitate and accelerate, as applicable, advanced research and development of security countermeasures (as defined in section 319F–2), qualified countermeasures (as defined in section 319F–1), or qualified pandemic or epidemic products (as defined in section 319F–3), that are applicable to the public health emergency or potential public health emergency under paragraph (1);

[...]

PRESIDENT BIDEN’S PLAN TO PROVIDE DIRECT RELIEF TO AMERICANS, CONTAIN COVID-19, AND RESCUE THE ECONOMY

The American Rescue Plan is delivering direct relief to the American people, rescuing the American economy, and starting to beat the virus. For a full overview of what’s in the plan, click here.

[...]

[...]

SEC. 313. <> PUBLIC AWARENESS CAMPAIGN ON THE IMPORTANCE OF VACCINATIONS.

(a) <> In General.--The Secretary, acting through the Director of the Centers for Disease Control and Prevention and in coordination with other offices and agencies, as appropriate, shall award competitive grants or contracts to one or more public or private entities to carry out a national, evidence-based campaign to increase awareness and knowledge of the safety and effectiveness of vaccines for the prevention and control of diseases, combat misinformation about vaccines, and disseminate scientific and evidence-based vaccine-related information, with the goal of increasing rates of vaccination across all ages, as applicable, particularly in communities with low rates of vaccination, to reduce and eliminate vaccine-preventable diseases.

[...]

§245. Public awareness campaign on the importance of vaccinations

(a) In general

The Secretary, acting through the Director of the Centers for Disease Control and Prevention and in coordination with other offices and agencies, as appropriate, shall award competitive grants or contracts to one or more public or private entities to carry out a national, evidence-based campaign to increase awareness and knowledge of the safety and effectiveness of vaccines for the prevention and control of diseases, combat misinformation about vaccines, and disseminate scientific and evidence-based vaccine-related information, with the goal of increasing rates of vaccination across all ages, as applicable, particularly in communities with low rates of vaccination, to reduce and eliminate vaccine-preventable diseases.

(b) Consultation

In carrying out the campaign under this section, the Secretary shall consult with appropriate public health and medical experts, including the National Academy of Medicine and medical and public health associations and nonprofit organizations, in the development, implementation, and evaluation of the evidence-based public awareness campaign.

(c) Requirements

The campaign under this section shall-

(1) be a nationwide, evidence-based media and public engagement initiative;

(2) include the development of resources for communities with low rates of vaccination, including culturally and linguistically appropriate resources, as applicable;

(3) include the dissemination of vaccine information and communication resources to public health departments, health care providers, and health care facilities, including such providers and facilities that provide prenatal and pediatric care;

(4) be complementary to, and coordinated with, any other Federal, State, local, or Tribal efforts, as appropriate; and

(5) assess the effectiveness of communication strategies to increase rates of vaccination.

(d) Additional activities

The campaign under this section may-

(1) include the use of television, radio, the internet, and other media and telecommunications technologies;

(2) include the use of in-person activities;

(3) be focused to address specific needs of communities and populations with low rates of vaccination; and

(4) include the dissemination of scientific and evidence-based vaccine-related information, such as-

(A) advancements in evidence-based research related to diseases that may be prevented by vaccines and vaccine development;

(B) information on vaccinations for individuals and communities, including individuals for whom vaccines are not recommended by the Advisory Committee for Immunization Practices, and the effects of low vaccination rates within a community on such individuals;

(C) information on diseases that may be prevented by vaccines; and

(D) information on vaccine safety and the systems in place to monitor vaccine safety.

The Public Readiness and Emergency Preparedness Act (PREPA), passed by the United States Congress and signed into law by President of the United States George W. Bush in December 2005 (as part of Pub.L. 109–148 (text) (PDF)), is a controversial tort liability shield intended to protect vaccine manufacturers from financial risk in the event of a declared public health emergency. The part of PREPA that actually affords such protection is now codified at 42 U.S.C. § 247d-6d. The act specifically affords to drug makers immunity from actions related to the manufacture, testing, development, distribution, administration and use of medical countermeasures against chemical, biological, radiological and nuclear agents of terrorism, epidemics, and pandemics. PREPA strengthens and consolidates the oversight of litigation against pharmaceutical companies under the purview of the secretary of Health and Human Services (HHS). PREPA provides $3.8 billion for pandemic influenza preparedness to protect public health in the case of a pandemic disease outbreak.

Vaccine manufacturers lobbied for the legislation, which would effectively preempt state vaccine safety laws in the case of an emergency declaration by HHS, by making clear they would not produce new vaccines unless the legislation was enacted.

During and in the aftermath of the 2020-21 COVID-19 pandemic in the United States, PREPA is being invoked in a variety of lawsuits, many involving skilled nursing or assisted living facilities where COVID-19 countermeasures including the administration or non-administration of vaccines is said to have resulted in or contributed to resident deaths.^[1] Although PREPA was around for more than 15 years, prior to COVID-19, the act's defensive application in litigation was not widespread, but now the application of the act is being included more frequently in a variety of COVID-19 related lawsuits, including Shareholder Derivative Litigation.^[2]

The Public Readiness and Emergency Preparedness Act (PREP Act) authorizes the Secretary of the Department of Health and Human Services (Secretary) to issue a PREP Act declaration. The declaration provides immunity from liability (except for willful misconduct) for claims:

• of loss caused, arising out of, relating to, or resulting from administration or use of countermeasures to diseases, threats and conditions
• determined by the Secretary to constitute a present, or credible risk of a future public health emergency
• to entities and individuals involved in the development, manufacture, testing, distribution, administration, and use of such countermeasures

[...]

The negotiators agreed to exactly $10 billion in offsets by tapping unspent funds from prior pandemic aid laws. The measure would claw back the following unused appropriations:

• $2.3 billion from a program intended to keep aviation manufacturing workers on payroll.
• $1.9 billion each from unused grans for shuttered live entertainment venues and a state small business credit program.
• $1.6 billion for Agriculture Department aid to commodity producers, food banks and others.
• $900 million for the Small Business Administration's econoic injury disaster loan program.
• $887 million from local and tribal assistance funds, with the addition of flexibility for state, localities and tribes to use existing funds for infrastucture-related spending, based on a Senate-passed bill from John Cornyn, R-Texas, and Alex Padilla, D-Calif.
• $500 million from aid to colleges and universities.

"Importantly, this bill is comprised of dollar-for-dollar offsets and will not cost the American people a single additional dollar," Sen. Mitt Romney, R-Utah, one of the lead GOP negotiators, said in a statement announcing the deal.

[...]

As a result of the continued consequences of the Coronavirus Disease 2019 (COVID-19) pandemic, on this date and after consultation with public health officials as necessary, I, Xavier Becerra, Secr​etary of Health and Human Services, pursuant to the authority vested in me under section 319 of the Public Health Service Act, do hereby renew, effective July 15, 2022, the January 31, 2020, determination by former Secretary Alex M. Azar II, that he previously renewed on April 21, 2020, July 23, 2020, October 2, 2020, and January 7, 2021, and that I renewed on April 15, 2021, July 19, 2021, October 15, 2021, January 14, 2022, and April 12, 2022, that a public health emergency exists and has existed since January 27, 2020, nationwide.

The US HHS Administrative state has extended the COVID medical emergency. Let's look at the data.

Senator Rand Paul has accused Dr. Fauci and the White House (which is captured by the HHS Administrative State) of “emotionalism and sensationalism” leading up to the renewal of the determination of a continuing medical emergency attributable to COVID-19 disease and SARS-CoV-2 infection.

Is this medical emergency justified, or does it reflect yet more mis- dis- and mal-information from the HHS Administrative state acting in coordination with corporate media to propagate Fearporn to justify the continuing suspension of medical ethics, normal regulatory process, censorship, and war profiteering by the medical-pharmaceutical industrial complex?

[...]

Per Epoch Times reporting:

“After White House adviser Dr. Anthony Fauci and Health and Human Services Secretary Xavier Becerra issued warnings about a new COVID-19 subvariant, Sen. Rand Paul (R-Ky.) said they are not providing key facts about the latest strain.

“How come the flu vaccine changes every year and they’re not willing to change this vaccine?” Paul told Fox News on Tuesday. “Now, you might have me with an argument. I’ll listen to you if you tell me, ‘We’ve got a new vaccine that actually has something to do with the current virus,'” he said.

It came after Fauci, who has given hundreds of media interviews since the start of the pandemic, told CNN this week that the Omicron subvariant BA.5 is concerning due to its high transmissibility. People infected in the first COVID-19 waves “really don’t have a lot of good protection” against the latest subvariant, Fauci also said at a White House briefing several days ago.

But Paul, himself a doctor, told Fox that Omicron “was about 90 percent less likely to put you in the hospital than the first variant,” saying that Americans should “discount” what both Fauci and Becerra are saying about the latest subvariant.

“So if no one’s telling you any information, how can you make any judgment other than the emotionalism and the sensationalism of the government?” he asked.”

Let’s look at the data using the slide format that so many seem to find useful. Minimal interpretation, mainly just data. I give you the tools, you make your own assessment and determination. What do you think is going on here?

[... see link for 15 slides ...]

The Biden administration on Thursday extended the nation’s COVID-19 public health emergency for the next 90 days as officials brace for a potential surge of infections over the winter.

The declaration comes as daily deaths and case rates have been falling, though the U.S. continues to see more than 300 people dying due to COVID-19 each day.

White House health officials have been urging people to get the updated variant-specific COVID-19 vaccine, and have said the extent of any surge depends on the precautions people take and the vaccination rates.

“If you are up to date with your vaccines and if you get treated, if you have a breakthrough infection, your risk of dying from COVID is now close to zero,” White House COVID-19 response coordinator Ashish Jha said Tuesday.

“We know there’s more work to do with real challenges ahead of us as we head into the fall and winter and the holidays. We’re doing everything we can as an administration to stay ahead of this virus. But if we all do our part — not just us in the administration, but Congress and the American people — I remain incredibly confident we can manage this virus for this fall and winter with less suffering and we can have a safe and healthy holiday season ahead,” Jha said.

The public health emergency was first declared in January 2020, and has been renewed every 90 days since.

[...]

As a result of the continued consequences of the Coronavirus Disease 2019 (COVID-19) pandemic, on this date and after consultation with public health officials as necessary, I, Xavier Becerra, Secretary of Health and Human Services, pursuant to the authority vested in me under section 319 of the Public Health Service Act, do hereby renew, effective October 13, 2022, the January 31, 2020, determination by former Secretary Alex M. Azar II, that he previously renewed on April 21, 2020, July 23, 2020, October 2, 2020, and January 7, 2021, and that I renewed on April 15, 2021, July 19, 2021, October 15, 2021, January 14, 2022, April 12, 2022, and July 15, 2022, that a public health emergency exists and has existed since January 27, 2020, nationwide.

Stop the Abuses of Power, Corruption, and Fiscal Irresponsibility

The National COVID-19 Emergency, first declared by President Trump in March 2020 in response to the COVID-19 pandemic, was formally extended a second time by President Biden on February 18, 2022 and will come up for a third consideration by Biden in February, 2023. In January 2020, the U.S. Department of Health and Human Services (HHS) declared a public health emergency (PHE) in response to the outbreak of COVID-19. Public health emergency declarations ease certain laws and regulations to make it easier to address the emergency and allow some federal grant money to flow toward addressing the emergency. A PHE is a lesser event than a national emergency, which triggers a rapid outlay of federal money to address the emergency. National emergencies also give great unliteral power to the president, allowing the president to do things such direct flows of money from the national treasury, deploy the national guard, etc.

From a clinical point of view from a physician who has treated COVID-19 from the very beginning, a PHE would be evident if hospital capacity was exceeded by COVID-19 patients and care could not be provided to other patients with urgent problems. As a general rule this would be >15% occupancy by COVID-19 patients. From that perspective, the COVID-19 PHE ended in January, 2021 once hospital capacity ramped up to meet demand. I checked the CDC website and the weekly cases of COVID-19 has maintained its unimpressive pattern of oscillations while hospitalized cases are about 5000 well below that 15% threshold of about 130,0000.

[...]

In summary, both national emergencies and PHE are power grabs that facilitate unchecked decisions and flows of money fostering corruption and continued desire to extend the declarations. The House and the Senate figured this out back in the 1970’s and found a legislative way of ending them. Until these declarations are dropped, we will continue to careen out of control on health policy, pandemic response, corruption, and fiscal irresponsibility. The most important question you can can ask a lawmaker, governor, or president or candidate: “Are you in favor of dropping the emergency declaration and PHE? If not why?

[...]

25 governors call on feds to ‘move on’ from pandemic, end COVID-19 public health emergency Kimberly Bonvissuto DECEMBER 21, 2022

November 22, 2022 Senate Approves Resolution to End COVID-19 National Emergency Declaration

Senate Stories | Reasserting Checks and Balances: The National Emergencies Act of 1976 July 1, 2021 By Senate Historical Office

What does the "intent to end" on May 11, 2023 actually mean for you?

Finally, we may be seeing a winding down of US Federal Government responses to the COVIDcrisis. January 30, 2023 is a date destined to go down in history as the beginning of the end of the draconian US Federal Government’s “public health” measures, which have been implemented in a step wise (ratcheting) manner beginning late January, 2020. What does this really mean, in a practical, real-world, kitchen-table sense of things?

Depending on when you define the point in time where SARS-CoV-2 entered the population of humans, the COVIDcrisis has extended for about three years- in contrast to the two year long “1918 Swine Flu” epidemic involving a different RNA respiratory virus attributed to causing over 50 million deaths world wide. As of January 31, 2023, there have been 6,812,798 cumulative deaths from COVID-19 per the WHO.

[...]

[...]

HHS Secretary Xavier Becerra sent a letter to U.S. governors with the surprise announcement. Becerra wrote:

"Based on current trends regarding COVID-19, the U.S. Department of Health and Human Services is planning for this to be the final renewal and for the COVID-19 PHE to end on May 11, 2023."

and

"Rather than 60 days' notice, I am providing 90 days' notice before the COVID-19 PHE ends to give you and your communities ample time to transition."

HHS appended a “fact sheet” to the letter with information on exactly what administrative and regulatory policies and rules will and will not be affected.

[...]

SUMMARY:

On February 9, 2023, the Secretary of Health and Human Services (HHS) renewed the Coronavirus Disease 2019 (COVID-19) public health emergency declaration issued under section 319 of the Public Health Service Act (PHS Act) (“PHE declaration”), effective February 11, 2023. The declaration is expected to expire at the end of the day on May 11, 2023. The Food and Drug Administration (FDA, Agency, or we) has issued guidance documents to address the circumstances of the public health emergency and, more generally, COVID-19. Many of those guidance documents are tied to the duration of the PHE declaration. This notice is intended to provide clarity to stakeholders with respect to the guidance documents that will no longer be effective with the expiration of the PHE declaration and the guidances that FDA is revising to continue in effect after the expiration of the PHE declaration.

[...]

E X E C U T I V E S U M M A R Y

I N T R O D U C T I O N

[...]

• Long-term Underinvestment in Public Health Infrastructure and Longstanding Health Disparities Put the Nation at Increased Risk from the Coronavirus.
• Before the Coronavirus Crisis, the United States Had Not Sufficiently Invested in Pandemic Preparedness, Despite Well-Known Risks.
• The Trump Administration’s Failed Stewardship Over the Pandemic Response and Persistent Pattern of Political Interference Undermined the Nation’s Ability to Respond to the Pandemic.
• The Toll of the Coronavirus Fell Disproportionately on the Most Vulnerable.
• Life-Saving Vaccinations and the Biden Administration’s Stewardship Helped the Nation Emerge from the Coronavirus Crisis, Yet Decisions Made by the Trump Administration, Actions Taken by Private Companies, and Predatory Actors Spreading Misinformation Have Undermined These Efforts.

[...]

• As the Coronavirus Crisis Upended the U.S. Economy, Longstanding Inadequate Protections for Workers Put America’s Families at Increased Risk.
• Congress Passed Rapid, Aggressive Federal Relief to Save Lives and Reduce Economic Damage, Which Compensated for Structural Weaknesses.
• The Trump Administration Failed to Prioritize and Effectively Deliver Relief for Working Americans.
• Poor Implementation and Oversight of Federal Aid Programs, Combined with Unscrupulous Private Actors, Led to Significant Waste, Fraud, and Abuse and a Less Effective Pandemic Response.
• Congress and the Biden Administration Improved the Federal Implementation of Pandemic Programs, Addressed Earlier Failures, and Supported a Robust and Equitable Jobs Recovery.

[...]

Tuesday, House Select Subcommittee on the Coronavirus Pandemic Chairman Brad Wenstrup from Ohio held a roundtable discussion titled “Preparing For the Future By Learning From the Past: Examining COVID Policy Decisions”. The goal of this roundtable, as stated on the House Oversight website, was to “discuss COVID-19 policy decisions with renowned doctors to thoroughly examine the federal government’s response to the COVID-19 pandemic.”

[...]

The Roundtable

The recently formed, bi-partisan COVID subcommittee kicked off its first roundtable discussion yesterday. There were witnesses brought by both Democrats and Republicans to answer questions and speak about their experiences through COVID.

The Panel:

Dr. Martin Kulldorff is an epidemiologist and biostatistician, as well as a Professor of Medicine (on leave) at Harvard. He is an original co-author of The Great Barrington Declaration, which advocated for focused protection as a strategy against COVID, instead of lockdowns in 2020.

Dr. Marty Makary is the Chief of Islet Transplant Surgery at Johns Hopkins, as well as a public health researcher and healthcare expert at John Hopkins University. Dr. Makary has over 250 peer-reviewed scientific articles and has been elected to the National Academy of Medicine.

Dr. Jay Battacharya is a Professor at Stanford School of Medicine. He’s been a champion for Medical Freedom since early on in the pandemic, and he was one of the first people to be censored on Twitter for his COVID views.

Dr. Georges Benjamin, the executive director of the American Public Health Association represented a defense of the government’s COVID response.

• Dr. Martin Kulldorfstarted off with a strong statement:
  “During the last few years, we have seen the worst public health mistakes in history”

https://twitter.com/VigilantFox/status/1630667108613759002?s=20

• Dr. Jay Battacharya addressed the widespread harms that occurred due to lockdowns, and the high number of COVID deaths even with harsh measures that trampled on civil liberties.
  “At best, they [lockdowns] temporarily protected the Laptop Class who could work from home without losing their jobs, about 30% of the population, while being served by the working class.”
  

https://twitter.com/VigilantFox/status/1631018021496946707?s=20

• Dr. Makary brought several crucial bits of information to light: He condemned the notion of injecting children.
  “Has any young, healthy child died in the United States of COVID? In the last three years?” he asked. “Germany did a study — it was zero kids, 5 through 11 years of age, that died that were healthy in that entire country.”

https://twitter.com/VigilantFox/status/1630668933559730176?s=20

• Dr. Makary mentioned the government’s decision to not recognize natural immunity. And to no one’s shock, Fauci played a big role in that decision.
  “He just decided … that if you have circulating antibodies that neutralize the virus, they’re antibodies the government does not recognize unless they were derived from the vaccine.”

[...]

[...]

Interestingly, the sanctimonious name-callers don’t seem to be even a tiny bit bothered by the $100 billion in revenue Pfizer recorded in 2022, the $2.82 million Dr. Fauci earned the year prior alone, or Bill Gates’ tone-deaf boast that his $10 billion investment in vaccines has seen a twenty to one return. They don’t care that hospitals get hefty bonus payments for every patient listed as having COVID-19 or put on a ventilator (a reality even USA Today’s patently weaponized “fact-checkers” had to admit is true), or get ruffled by the hundreds of millions of federal dollars individual school districts across the country accepted to enforce mask and vaccine requirements on students. Nope, it’s doctors like Kory—for whom incidentally it is a felony to accept monetary compensation for prescribing medications—who are the real pandemic profiteers. (And if you come at me with any sort of “books make people millionaires” ignorance, I’ll gladly torture you with a painful lesson in publishing accounting.)

[...]

• Congress has approved some $4.5 trillion in total aid spending. Federal agencies have formally committed to using about $4 trillion of that, and have made $3.5 trillion in actual payments to date.
• It can often take time for the total pot of funds approved by lawmakers to make its way to the American people, budget experts say.
• Education, health care and disaster relief are among the areas where the government has underspent the funds, according to a CNBC analysis.

[...]

[...]

Historically (as was the case in World War II) a crisis typically arose in the form of an aggressive foreign power. James Madison observed that the trouble with an established military interest is that, because it accrues its wealth, power, glory, and prestige from waging war, it is necessarily interested in waging wars instead of averting them.

The same can now be said of emerging infectious diseases. Instead of armed soldiers threatening us, we are menaced by invisible pathogens. Instead of Lockheed Martin and Raytheon receiving the federal money gravy train, it’s Pfizer, Moderna, and the rest of the Bio-Pharmaceutical Complex that has been positioning itself for the next (“certain to emerge”) infectious disease.

The legal framework for this bonanza was established by the PREP Act (Public Readiness and Emergency Preparedness) of 2005. This authorized the Secretary of Health and Human Services to deploy a wide array of “Emergency Countermeasures” in the event of an infectious disease outbreak. When invoked by the HHS Secretary, the PREP Act provides immunity for the “manufacture, testing, development, distribution, administration, and use of covered countermeasures.” On February 4, 2020, HHS Secretary Alex Azar declared COVID-19 an emergency and invoked the PREP Act.

Pursuant to the PREP Act, the CARES Act of March 27, 2020—passed within the context of a “public health emergency”—created $2 trillion with the stroke of a keyboard. These funds were disbursed to a host of companies, individuals, and institutions in the business of infectious disease “countermeasures.” The Act was reminiscent of the Emergency Economic Stabilization Act of 2008 for bailing out Wall Street.

Because the mRNA vaccines fall under the PREP Act definition of “emergency countermeasures,” their production is not subjected to the same testing and quality control regulations as licensed pharmaceutical products. Their production and deployment resemble that of military products during World War II. For example, many aircraft hastily designed and manufactured for that cataclysm were so dangerous and unreliable that far more servicemen were killed in training and routine flight accidents than in combat. The fabled Vought F4U Corsair was known as the “Ensign Eliminator” because its dreadful stall characteristics killed so many young airman.

[...]

Since the start of the coronavirus pandemic, Congress, states, and both the Trump and Biden Administrations have adopted a number of policies to ease financial pressure on hospitals and other health care providers. The infusion of funds was intended to help alleviate the fiscal impact of revenue loss due to delays in non-urgent care, coupled with new costs associated with COVID-19. With the recent increase in Omicron-related cases, hospitalizations and deaths, this brief describes the main sources of federal funds for health care providers and how those funds have been allocated. It also describes federal spending for COVID-19 testing, including at-home testing, using the most recent data available (as of September 2021).

Federal Funding for Hospitals and Other Health Care Providers During the Pandemic:
Key Sources of Federal Support

• Congress established the Provider Relief Fund to bolster hospitals and other health care providers to compensate for financial losses and unanticipated costs during the pandemic. HHS has allocated $170.9 billion of the total $178 billion authorized by Congress for this Fund as of September 2021, including $14.8 billion used to support vaccine development and distribution. Of the total amount, $143 billion has been disbursed, according to GAO and HHS announcements. HHS expects to distribute another $6 billion to providers in early 2022.
• In addition, $7.5 billion of $8.5 billion in American Rescue Plan (ARP) rural funds were distributed to hospitals and other providers that serve patients living in rural areas; the remaining $1 billion in rural funds is expected to be distributed in early 2022.
• Congress took several steps to avoid automatic payment reductions during the pandemic. Congress waived the automatic 2% reduction in Medicare payments required under budget rules (i.e., sequestration) between May 1, 2020 and March 31, 2022, delayed until 2023 a separate 4% reduction in Medicare payments that would otherwise have been triggered in 2022 under PAYGO rules, and increased physician payments by 3% for 2022 under the Medicare Physician Fee Schedule (PFS) payments to mitigate scheduled budget neutral cuts.
• Congress established the Paycheck Protection Program that provided health care providers an estimated $100 billion in Paycheck Protection Program (PPP) loans, according to MedPAC.
• In addition, Congress increased Medicare payments for inpatient COVID-19 admissions by 20% during the public health emergency (PHE), established coverage and payment for administering COVID-19 vaccines, and increased payments for telehealth services, and HHS waived certain regulatory restrictions, such as allowing for expanded coverage of Medicare telehealth services. Congress also provided accelerated or advance payments as loans to providers participating in traditional Medicare to ease cash flow disruptions during the pandemic.

[...]

• Reimbursement for COVID-19 vaccination administration: Medicare increased its reimbursement for COVID-19 vaccine administration from $17 for an initial dose in a series and $28 for the final dose in a series to approximately $40 per dose. This also applies to booster doses approved by the FDA under the emergency use authorizations. As of June 2021, Medicare also pays an additional $35 per dose for administering the COVID-19 vaccine in the home for certain Medicare patients. Most states have policies in place to increase Medicaid payments for COVID-19 vaccine administration to 100% of the Medicare rate. Medicare and Medicaid beneficiaries are not subject to any cost sharing for the COVID-19 vaccine and administration. For the uninsured and underinsured, a portion of the Provider Relief Funds are being used to reimburse providers for administering COVID-19 vaccines to uninsured or underinsured individuals.

[...]

The claim: Hospitals get paid more if patients are listed as COVID-19, and on ventilators

Sen. Scott Jensen, R-Minn., a physician in Minnesota, was interviewed by "The Ingraham Angle" host Laura Ingraham on April 8 on Fox News and claimed hospitals get paid more if Medicare patients are listed as having COVID-19 and get three times as much money if they need a ventilator.

The claim was published April 9 by The Spectator, a conservative publication. WorldNetDaily shared it April 10 and, according to Snopes, a related meme was shared on social media in mid-April.

Jensen took it to his own Facebook page April 15, saying, in part:

"How can anyone not believe that increasing the number of COVID-19 deaths may create an avenue for states to receive a larger portion of federal dollars. Already some states are complaining that they are not getting enough of the CARES Act dollars because they are having significantly more proportional COVID-19 deaths."

[...]

Our ruling: True

We rate the claim that hospitals get paid more if patients are listed as COVID-19 and on ventilators as TRUE.

Hospitals and doctors do get paid more for Medicare patients diagnosed with COVID-19 or if it's considered presumed they have COVID-19 absent a laboratory-confirmed test, and three times more if the patients are placed on a ventilator to cover the cost of care and loss of business resulting from a shift in focus to treat COVID-19 cases.

[...]

[...]

As exposed in audio recordings, hospital executives in Arizona admitted meeting several times a week to lower standards of care, with coordinated restrictions on visitation rights. Most COVID-19 patients’ families are deliberately kept in the dark about what is really being done to their loved ones.

The combination that enables this tragic and avoidable loss of hundreds of thousands of lives includes (1) The CARES Act, which provides hospitals with bonus incentive payments for all things related to COVID-19 (testing, diagnosing, admitting to hospital, use of remdesivir and ventilators, reporting COVID-19 deaths, and vaccinations) and (2) waivers of customary and long-standing patient rights by the Centers for Medicare and Medicaid Services (CMS).

[...]

Creating a “National Pandemic Emergency” provided justification for such sweeping actions that override individual physician medical decision-making and patients’ rights. The CARES Act provides incentives for hospitals to use treatments dictated solely by the federal government under the auspices of the NIH. These “bounties” must paid back if not “earned” by making the COVID-19 diagnosis and following the COVID-19 protocol.

The hospital payments include:

• A “free” required PCR test in the Emergency Room or upon admission for every patient, with government-paid fee to hospital.
• Added bonus payment for each positive COVID-19 diagnosis.
• Another bonus for a COVID-19 admission to the hospital.
• A 20 percent “boost” bonus payment from Medicare on the entire hospital bill for use of remdesivir instead of medicines such as Ivermectin.
• Another and larger bonus payment to the hospital if a COVID-19 patient is mechanically ventilated.
• More money to the hospital if cause of death is listed as COVID-19, even if patient did not die directly of COVID-19.
• A COVID-19 diagnosis also provides extra payments to coroners.

[...]

Congress set up a massive, $178 billion fund in 2020 meant to help mitigate the impacts of the Covid-19 pandemic on health care providers, known as the Provider Relief Fund.

The Trump and Biden administrations haven’t always been reliable about sending out the money — or sending it on time. But STAT’s new analysis of a Health and Human Services database of the money reveals where it’s flowing and who has received the most so far.

By far, the largest payments were made to the nation’s biggest hospital systems. Fully five of the top 10 recipients of cash were New York City-area hospitals or health systems; together, they received some $3.1 billion. The New York and Presbyterian Hospital (usually styled “NewYork-Presbyterian”) alone brought in $631 million, topped only by the $1.2 billion that went to the New York City Health and Hospitals Corporation, a group that operates New York City’s sprawling system of public hospitals and clinics.

STAT is publishing the entire database here in a searchable and sortable format.

Many smaller providers also benefited from the program. Of the 412,591 payments published so far, the median was just $12,530. Ninety percent of all payments were below $192,569.

[...]

April 08, 2020 - Hospital reimbursement for the treatment of uninsured COVID-19 patients could account for more than 40 percent of the $100 billion earmarked for hospitals in the latest coronavirus stimulus package, according to estimates from the Kaiser Family Foundation.

In a new issue brief, researchers from the Kaiser Family Foundation estimated total hospital reimbursement to range from $13.9 billion to $41.8 billion depending on the rate of and severity of COVID-19 hospitalizations among the uninsured population.

That reimbursement range is based on Medicare reimbursement for hospitals admissions for similar conditions, including respiratory infections and inflammations with major comorbidities or complications, which averaged $13,297 in reimbursements, and, in more severe cases, respiratory system diagnosis with ventilator support for greater than 96 hours, which averaged $40,218.

Researchers also estimated that up to 2 million uninsured individuals could require hospitalization for COVID-19. Although, that number could be as low as 670,000 hospitalizations.

[...]

CMS issued an Interim Final Rule with Comment Period that established the New COVID-19 Treatments Add-on Payment (NCTAP) under the Medicare Inpatient Prospective Payment System (IPPS). The NCTAP, designed to mitigate potential financial disincentives for hospitals to provide new COVID-19 treatments, is effective from November 2, 2020, until the end of the COVID-19 public health emergency (PHE).

Through the NCTAP, the Medicare Program will provide an enhanced payment for eligible inpatient cases that use certain new products with current FDA approval or emergency use authorization (EUA) to treat COVID-19, including the following:

• On August 23, 2020, the FDA issued (reissued on November 30, 2020, and revised on March 9, 2021) an EUA for the use of COVID-19 convalescent plasma for treating COVID-19 in hospitalized patients
• On October 22, 2020, the FDA approved remdesivir (Veklury) for the treatment of COVID-19 for adults and certain pediatric patients requiring hospitalization
• On November 19, 2020, the FDA issued (and amended on December 20, 2021) an EUA for the use of baricitinib (Olumiant) for the treatment of suspected or laboratory confirmed COVID-19 in certain hospitalized patients
• On December 22, 2021, the FDA issued an EUA for molnupiravir for the treatment of mild-to-moderate COVID-19 in certain adults who are at high-risk for progression to severe COVID-19, including hospitalization or death.
• On December 23, 2021, the FDA issued an EUA for nirmatrelvir (Paxlovid) for the treatment of mild-to-moderate COVID-19 in certain adults and pediatric patients at high risk for progression to severe COVID-19, including hospitalization or death. 
   

For eligible cases, the NCTAP is equal to the lesser of these:

• 65% of the operating outlier threshold for the claim
• 65% of the amount by which the costs of the case exceed the standard Diagnosis-Related Group (DRG) payment (including the adjustment to the relative weight under Section 3710 of the Coronavirus Aid, Relief, and Economic Security Act (CARES Act)

Coding for NCTAP

NCTAP claims are those that are eligible for the 20% add-on payment under Section 3710 of the CARES Act. Eligible claims have an ICD-10-CM diagnosis code U07.1 (COVID-19) and one of the following:

• ICD-10-PCS codes for remdesivir (Veklury), COVID-19 convalescent plasma, or baricitinib (Olumiant).
• National Drug Codes (NDC) for nirmatrelvir and molnupiravir

Codes for Remdesivir or COVID-19 Convalescent Plasma for Hospital Discharges on or after November 2, 2020

[...Table of codes follows...]

Upon admission to a once-trusted hospital, American patients with COVID-19 become virtual prisoners, subjected to a rigid treatment protocol with roots in Ezekiel Emanuel’s “Complete Lives System” for rationing medical care in those over age 50. They have a shockingly high mortality rate. How and why is this happening, and what can be done about it?

As exposed in audio recordings, hospital executives in Arizona admitted meeting several times a week to lower standards of care, with coordinated restrictions on visitation rights. Most COVID-19 patients’ families are deliberately kept in the dark about what is really being done to their loved ones.

The combination that enables this tragic and avoidable loss of hundreds of thousands of lives includes (1) The CARES Act, which provides hospitals with bonus incentive payments for all things related to COVID-19 (testing, diagnosing, admitting to hospital, use of remdesivir and ventilators, reporting COVID-19 deaths, and vaccinations) and (2) waivers of customary and long-standing patient rights by the Centers for Medicare and Medicaid Services (CMS).

In 2020, the Texas Hospital Association submitted requests for waivers to CMS. According to Texas attorney Jerri Ward, “CMS has granted ‘waivers’ of federal law regarding patient rights. Specifically, CMS purports to allow hospitals to violate the rights of patients or their surrogates with regard to medical record access, to have patient visitation, and to be free from seclusion.” She notes that “rights do not come from the hospital or CMS and cannot be waived, as that is the antithesis of a ‘right.’ The purported waivers are meant to isolate and gain total control over the patient and to deny patient and patient’s decision-maker the ability to exercise informed consent.”

Creating a “National Pandemic Emergency” provided justification for such sweeping actions that override individual physician medical decision-making and patients’ rights. The CARES Act provides incentives for hospitals to use treatments dictated solely by the federal government under the auspices of the NIH. These “bounties” must be paid back if not “earned” by making the COVID-19 diagnosis and following the COVID-19 protocol.

The hospital payments include:

• A “free” required PCR test in the Emergency Room or upon admission for every patient, with government-paid fee to hospital.
• Added bonus payment for each positive COVID-19 diagnosis.
• Another bonus for a COVID-19 admission to the hospital.
• A 20 percent “boost” bonus payment from Medicare on the entire hospital bill for use of remdesivir instead of medicines such as Ivermectin.
• Another and larger bonus payment to the hospital if a COVID-19 patient is mechanically ventilated.
• More money to the hospital if cause of death is listed as COVID-19, even if patient did not die directly of COVID-19.
• A COVID-19 diagnosis also provides extra payments to coroners.

CMS implemented “value-based” payment programs that track data such as how many workers at a healthcare facility receive a COVID-19 vaccine. Now we see why many hospitals implemented COVID-19 vaccine mandates. They are paid more.

[...]

As reported last week by The Defender, federal monies from the 2020 and 2021 COVID stimulus bills dramatically reshaped K-12 educational priorities, turning American school officials into lackeys for federal agencies more intent on masking and vaccinating every last child than on supporting meaningful education.

So, too, with the stimulus-induced reshaping of hospital priorities.

In the second half of a January interview on Del Bigtree’s “The Highwire” — “COVID-19: Following the Money” — policy analyst A.J. DePriest reported on the untoward consequences set into motion as a result of COVID funds provided to hospitals.

Managed by the U.S. Department of Health and Human Services (HHS), the federal government allocated a total of $186.5 billion to the Provider Relief Fund (PRF), with two-thirds ($121.3 billion) disbursed as of January 2022.

The first tranche of $50 billion for hospitals and other Medicare providers — “for healthcare-related expenses or lost revenues … attributable to COVID-19” — began flying out the door in April 2020.

Almost immediately, alert doctors and astute journalists warned the Medicare add-on payments built into the relief package created perverse incentives unfriendly to patients’ interests.

As summarized by Dr. Scott Jensen — former Minnesota state senator and current gubernatorial candidate — “anytime healthcare intersects with dollars it gets awkward.”

Nearly two years down the road, the “awkwardness” is increasingly difficult to hide.

In the view of DePriest and many others, HHS’s stimulus slush fund has been every bit as dangerous for hospital patients as the U.S. Department of Education’s handouts have been for the nation’s schoolchildren.

Making out like bandits

Dr. Elizabeth Lee Vliet and Ali Shultz, J.D., who wrote a widely distributed op-ed in late 2021 for the Association of American Physicians and Surgeons (AAPS), summed up the disturbing situation prevailing in hospitals. The AAPS’s professional calling card is its “dedication to the highest ethical standards of the Oath of Hippocrates.”

Not mincing their words, the two argued that Centers for Medicare and Medicaid Services (CMS) payment directives turned hospitals and medical staff into “bounty hunters,” and COVID patients into “virtual prisoners.”

Highlighting the slew of CMS add-ons and other incentives established with the Coronavirus Aid, Relief and Economic Security (CARES) Act — and also the Paycheck Protection Program and Health Care Enhancement Act (PPPHCEA) — they emphasized the payments hinge on hospitals’ willingness to slavishly follow the National Institutes of Health’s (NIH’s) guidelines “for all things related to COVID-19.”

As itemized by Vliet and Shultz, compliant hospitals garner CMS payments for:

• Each completed diagnostic test (required in the emergency room or upon admission).
• Each COVID-19 diagnosis.
• Each COVID admission.
• Use of the intravenously administered Gilead drug remdesivir (brand name Veklury), which yields a 20% bonus payment on the entire hospital bill.
• Mechanical ventilation.
• COVID-19 listed as cause of death.

Citing a Becker’s Hospital Review breakdown, published in April 2020, of CARES Act payments to different states, DePriest told Bigtree payments ranged from $166,000 per COVID patient in Tennessee hospitals, for example, to far higher payments in states such as North Dakota ($339,000), Nebraska ($379,000) and West Virginia ($471,000).

In addition, for hospitals ascertained to be in COVID “hotspots,” HHS distributed special “high-impact” funds — $77,000 per admission initially, later downsized to $50,000 per admission.

HHS explained it used COVID admissions “as a proxy for the extent to which each facility experienced lost revenue and increased expenses associated with directly treating a substantial number of COVID-19 inpatient admission [sic].

[...]

The claim: Blue Cross Blue Shield pays doctors bonuses based on the number of patients vaccinated

In an attempt to cast doubt on the safety and efficacy of COVID-19 vaccines, some online users are claiming pediatricians are paid a bonus by Blue Cross Blue Shield based on the percentage of patients they vaccinate.

“Blue Cross Blue Shield pays your doctor a $40,000 bonus for fully vaccinating 100 patients under the age of 2,” reads a Dec. 12, 2021, Instagram post that was shared by actress Cherie Johnson and accumulated more than 600 likes. “If your doctor manages to fully vaccinate 200 patients, that bonus jumps to $80,000.”

The post claims pediatricians lose the entire bonus unless at least 63% of patients are fully vaccinated, including the flu vaccine. It asserts, "This is why your doctor gets aggressive."

But Blue Cross Blue Shield doesn't provide incentives solely based on the number of patients vaccinated, as the post suggests. Incentive programs vary by state and require doctors to meet goals related to a number of different practices and services.

Bonuses not based solely on vaccines

Blue Cross and Blue Shield is a national federation of 35 independent and locally operated companies, each of which sets its own value-based contracts with local providers, according to an agency spokesperson.

“The purpose of any performance-based incentives, where they exist, is to reward implementation of well-established, evidence-based best practices in the care of our members,” a Blue Cross Blue Shield spokesperson said in an emailed statement. “While vaccinations may fall into that category, they would not be the sole performance measure.”

[...]

Our rating: Missing context

[...]

[...]

But the riches get even richer for physicians during COVID-19!

A second incentive program was based on a bonus system for percent of patients vaccinated during the 2021 year. That document is as follows:

With an average patient to primary care physician ratio of 1800, lets do the numbers for the 2021 final incentive program for the seven month period (.58% of 12 months) beginning on January 1, 2021. Note: these are examples, based on 1800 a patient practice per physician.

• 30% of anthem members vaccinated within a practice x $20 (x .58) = $10,800.00

• 40% of anthem members vaccinated within a practice x $45 = $32,400.00

• 50% of anthem members vaccinated within a practice x $70 = $63,000.00

• 60% of anthem members vaccinated within a practice x $100 = $108,000.00

• 75% of anthem members vaccinated within a practice x $125 = $168,750.00

  ---

With a patient to primary care physician ratio of 1800, lets do the numbers for the 2021 final incentive program (which would have included children 12 and up) for the FIVE month period (.41% of 12 months) at the end of 2021.

• 30% of anthem members vaccinated within a practice x $100 (x .41) = $22,140

• 40% of anthem members vaccinated within a practice x $150 = $44,280.00

• 50% of anthem members vaccinated within a practice x $175 = $64,575.00

• 60% of anthem members vaccinated within a practice x $200 = $88,560.00

• 75% of anthem members vaccinated within a practice x $250 = $138,375.00

It appears that during 2021, the individual bonus plan and the percent vaccinated “incentive” program ran simultaneously.

If a practice managed to achieve a 75% vaccination rate, the bonus and incentive program would have yielded an extra profit somewhere in the range of $382,125.00 for 2021!

My example calculations (each practice numbers would vary):

[...]

You might recall that back in the very early days of Covid-19 (or just “coronavirus” as it was then known), some crypto nutters enthusiasts started getting excited about the idea that the virus would be good for bitcoin because “paper money” “might be the source of #CORONAVIRUS #SARS2 infection”. After all, “fiat is dirty”:

[...]

Now, to be fair to the bitcoin bros (not great) and XRP army (worse), even the World Health Organisation had around that time started pushing the idea that Covid could be being spread by banknotes (while simultaneously recommending that people should not wear masks), now thought to be “very unlikely”. Even if banknotes were a key transmission vector, however, we are not sure that “dirty fiat” itself could be held responsible, given that the vast majority of it only exists in digital form. Why would you use bitcoin, or XRP, or any other crypto token when you can transact digitally using fiat currencies? Yet in some ways, the crypto crowd were not wrong. In the almost 18 months since Covid-19 was declared a pandemic, the price of bitcoin has risen by about 525 per cent, from just under $8,000 to a three-month high just above $50,000 on Monday. XRP has climbed by a similar amount to trade around the $1.25 mark.

[...]

“COVID fraud” is at this point a redundant phrase. Congress appropriated more than $5 trillion for COVID relief but almost $600 billion may have been lost to fraud — an astounding 12%. Washington’s pandemic pratfalls are the greatest federal boondoggle of this century.

Prosecutors are having a turkey shoot nailing COVID crooks: More than 1,500 have been indicted and almost 500 have been convicted. On September 14, the Justice Department announced the creation of three COVID-19 fraud strike force teams.

When President Biden recently signed a law to extend the time to prosecute COVID fraud, he declared, “My message to those cheats out there is this: You can’t hide. We’re going to find you.” But the sheer amount of fraud makes it unlikely that the vast majority of thieves will be charged.

Policymakers acted as if waiving standard federal fraud protections would somehow thwart the COVID virus. On September 22, the Labor Department inspector general estimated that COVID-19 unemployment fraud amounted to $45 billion and could exceed $163 billion. “Overseas organized crime groups flooded state unemployment systems with bogus online claims, overwhelming antiquated computer software benefits in blunt-force attacks that siphoned out millions of dollars,” NBC News reported.

Prison inmates, drug gangs and Nigerian racketeers easily plundered the program. One swindler collected unemployment benefits from 29 different states. In the first year of the pandemic, Maryland detected more than 1.3 million fraudulent unemployment claims — equal to 20% of the state’s population.

Beginning in June 2020, the feds distributed $813 billion in Paycheck Protection Program loans to businesses. President Donald Trump’s Treasury Secretary Steven Mnuchin boasted that PPP is “supporting an estimated 50 million jobs.” But many of those jobs existed solely in the imagination of political appointees.

The Small Business Administration (SBA), which administered the program, effectively told people, “Apply and sign and tell us that you’re really entitled to the money,” according to Justice Department Inspector General Michael Horowitz. The SBA camouflaged its “don’t ask, don’t tell” loan standard by claiming to perform economic miracles. The SBA ludicrously boasted that PPP loans saved more jobs than the total number of employees in at least 15 industries.

Yet CBS News found that PPP loans had gone to more than a thousand “ghost businesses” in Markham, Illinois — indicative of a nationwide problem of deluging non-existent companies with federal cash. The feds gave “loans to 342 people who said their name was ‘N/A,’” the New York Times reported.

Fraud permeated relief programs of practically every federal agency that gushered money. On September 20, the feds charged 47 people in Minnesota with looting $250 million from the federal child nutrition programs’ COVID aid. Prosecutors denounced the “brazen scheme of staggering proportions” but federal and state bureaucrats should have stopped the pilfering from the start. “Feeding Our Future,” a nonprofit organization, pocketed $300,000 in subsidies in 2018 and a windfall of almost $200 million in 2021. Fraud snowballed because the US Department of Agriculture issued waivers to “suspend all on-site monitoring of providers” of children’s meals.

Instead of feeding hungry kids, tax dollars were pilfered using a list of phony recipients generated by the website listofrandomnames.com. (No wonder Feeding Our Future wasn’t invited to attend Biden’s White House Summit on Hunger last week.) When the state of Minnesota sought to cut off funding, Feeding Our Future sued, claiming the action “discriminated against a nonprofit that worked with racial minorities,” the Minneapolis Star Tribune reported. Leftist firebrand Rep. Ilhan Omar (D-Minn.) received thousands of dollars in donations from individuals indicted in the scandal.

Fighting fraud is tricky for federal investigators when some politicians openly used COVID stimulus money to bribe voters. In the January 2021 Georgia runoff race for US Senate, the campaign of Democratic candidate Raphael Warnock distributed fliers declaring, “Want a $2,000 Check? Vote Warnock.” That promise helped Warnock win, sealing Democratic control of the Senate and opening the floodgates for trillions of dollars of additional Biden administration spending.

[...]

Thousands of officials across the government’s executive branch reported owning or trading stocks that stood to rise or fall with decisions their agencies made, a Wall Street Journal investigation has found.

More than 2,600 officials at agencies from the Commerce Department to the Treasury Department, during both Republican and Democratic administrations, disclosed stock investments in companies while those same companies were lobbying their agencies for favorable policies. That amounts to more than one in five senior federal employees across 50 federal agencies reviewed by the Journal.

Some sold in January 2020 when the government began mobilizing against the threat. Others bought shares as a market-rescue plan was taking shape.

Federal officials working on the government response to Covid-19 made well-timed financial trades when the pandemic began—both as the markets plunged and as they rallied—a Wall Street Journal investigation found.

In January 2020, the U.S. public was largely unaware of the threat posed by the virus spreading in China, but health officials were on high alert and girding for a crisis.

[...]

In a shocking new report from the Wall Street Journal, leading health officials began offloading stocks at truly unprecedented rates in January 2020—well before the COVID-19 emergency was declared—with officials at the US Department of Health and Human Services selling 60% more stocks in January 2020 than average over the previous 12 months.

One deputy to NIAID Director Anthony Fauci reported selling between $157,000 and $480,000 in stocks before the end of January.

Weeks later, stock prices around the world went into freefall at the fastest rate since the Great Depression as word got round that officials were planning a complete shutdown of the global economy.

The ensuing lockdowns were unprecedented in the western world prior to Xi Jinping’s lockdown of Wuhan and weren’t part of any democratic country’s pandemic plan. They weren’t given any official imprimatur as western policy until February 24, 2020, when WHO Assistant Director-General Bruce Aylward—famous for later disconnecting a live interview when asked to acknowledge Taiwan—reported back about Wuhan’s lockdown from Beijing:

What China has demonstrated is, you have to do this. If you do it, you can save lives and prevent thousands of cases of what is a very difficult disease.

That leading officials were already privately planning to recreate China’s lockdowns across the western world by January 2020, however—and making stock trades based on those plans—further confirms the all-too-prescient stock tip by someone who claimed to have “friends and family in the medical industry and field, including at CDC and one close friend at WHO” on January 30, 2020, which proved to be a near-perfect foretelling of subsequent events:

There are very high profile investors who've been silently pulling out ahead of time… the WHO is already talking about how ‘problematic’ modeling the Chinese response in Western countries is going to be, and the first country they want to try it out in is Italy. If it begins a large outbreak in a major Italian city they want to work through the Italian authorities and world health organizations to begin locking down Italian cities in a vain attempt to slow down the spread at least until they can develop and distribute vaccines, which btw is where you need to start investing.

AHIP Study Finds Top Drug Companies’ Sales and Marketing Budgets Swamp R&D Budgets

In case you missed it, America’s Health Insurance Plans (AHIP) released a new study Wednesday that found Big Pharma continued to spend more advertising and selling its products than investing in research and development (R&D) even amid unprecedented focus on the development of new treatments as a result of the COVID-19 pandemic.

The study found that “Of the 10 drug manufacturers examined, 7 of them spent more on selling and marketing expenses than they did on research and development. For this group of 10 companies alone, selling and marketing expenses exceeded R&D spending by $36 billion, or 37%.” AHIP emphasized that, “this use of dollars occurred during a year dedicated to the development of new treatments and vaccines to overcome the COVID-19 crisis.”

The study shows that brand name drug manufacturers including AbbVie, Pfizer, Novartis, GlaxoSmithKline, Sanofi, Bayer and Johnson & Johnson all spent more on marketing and selling their products in 2020 than they did on developing new treatments:

• AbbVie spent $11 billion on sales and marketing in 2020, compared to $8 billion on R&D.
• Pfizer spent $12 billion on sales and marketing, compared to $9 billion on R&D.
• Novartis spent $14 billion on sales and marketing, compared to $9 billion on R&D.
• GlaxoSmithKline spent $15 billion on sales and marketing, compared to $7 billion on R&D.
• Sanofi spent $11 billion on sales and marketing, compared to $6 billion on R&D.
• Bayer spent $18 billion on sales and marketing, compared to $8 billion on R&D.
• Johnson & Johnson spent $22 billion on sales and marketing, compared to $12 billion on R&D.

“Big Pharma’s practices clearly show that their growth strategy is based on selling a greater volume of drugs to patients – not on creating groundbreaking new therapies and delivering more value to patients,” AHIP wrote, concluding that, “With thoughtful solutions that encourage private-market competition and end pharma’s gaming of the system, we can have both.”

[...]

The COVID-19 crisis presented ripe opportunities for fraudsters and swindlers to exploit the system.

The COVID-19 pandemic, which placed unprecedented demands on federal financial assistance programs, also presented ripe opportunities for fraudsters and swindlers to exploit the system.

A report released by the Department of Justice (DOJ) COVID-19 Fraud Enforcement Task Force uncovered a shocking scope of fraud during the pandemic, with over $400 billion in emergency funding either stolen or misappropriated.

According to the report, fraudulent claims and schemes targeted various pandemic relief efforts, including unemployment insurance benefits, Paycheck Protection Program (PPP) loans, and Economic Injury Disaster Loans (EIDLs), among others.

These included fraudulent claims filed using stolen identities, inflated payroll expenses, doctored bank statements, and false tax forms.

The report reveals that fraudsters and swindlers may have stolen upwards of $280 billion in emergency funding, with an additional $123 billion lost or misappropriated, totaling more than $400 billion in funds intended to aid Americans during one of the most challenging times in recent history, The Politics Brief reported.

Here are some examples of COVID-19 fraud cases:

A defendant was sentenced to seven years in federal prison for committing PPP, EIDL, and UI fraud, with actual losses of more than $1 million and attempted losses of $3 million. When the government executed search warrants in the case, agents recovered stolen identifying information and ghost guns, including one modified to function as a machine gun.

A defendant pleaded guilty to submitting more than $3.5 million in fraudulent COVID-19 PPP and EIDL applications and using fraudulently obtained funds to pay for a vacation, a Mercedes-Benz, jewelry, and luxury goods, including items from Luis Vuitton, Neiman Marcus, Dior, Cartier, Gucci, Chanel, and Hermes.

The SDFL indicted 17 employees of the Broward Sheriff’s Office were charged with obtaining fraudulent PPP/ EIDL loans. One former deputy was recently convicted at trial, several employees have pleaded guilty, and other defendants’ cases are still pending.

A defendant was sentenced to 71 months in prison for fraudulently obtaining PPP and EIDL loans and Shuttered Venue Operator Grants (SVOG), using the stolen funds to buy two Tesla S models, a Lamborghini, a Porsche, a diamond Audemars Piguet watch, a rose gold and diamond pendant with his company’s logo, a half-kilogram gold chain with 70 carats of diamonds, and a 1-kilogram gold chain.

A former contract detention officer at the federal Krome Detention facility who was the leader of a PPP fraud ring was sentenced to 32 months in prison for preparing fraudulent PPP applications in return for kickbacks.

A defendant was sentenced to 70 months in prison for laundering the over $2 million in fraudulently obtained PPP and EIDL loans and using the funds to gamble and to pay for cosmetic surgery, a Cadillac Escalade, and a Pomeranian puppy.

In the Southern District of Georgia, a Florida-based attorney was convicted at trial of conspiracy to fraudulently obtain almost $800,000 in Economic Injury Disaster Loans for herself and others.

In the Western District of Washington, the ringleader of a $6.8 million pandemic fraud ring was sentenced to five years in prison for fraudulently seeking funds from various relief programs.

In the Eastern District of Washington, an Arkansas-based business owner pleaded guilty to fraudulently receiving more than $16.5 million in SBApandemic relief funds for himself and others.

In the Eastern District of Virginia, a former VA nurse was sentenced to 18 years in prison for conspiring to fraudulently obtain more than $3.5 million in UI benefits from at least five states. She and her co-conspirators filed more than 220 false applications for unemployment insurance benefits using stolen identities and the identities of state and federal prison inmates.

In the Middle District of Florida, a defendant was sentenced to eight years and six months in prison for obtaining more than $7.2 million in PPP loan funds, which he used to purchase Maserati and Mercedes-Benz cars and buy a 12-acre estate.

The District of Minnesota has brought charges against more than 50 individuals for their respective roles in a $250 million fraud scheme that exploited a federally funded child nutrition program during the COVID-19 pandemic.

In the Eastern District of Michigan, a man was sentenced to 15 years in prison for his role as the ringleader of conspiracies to use stolen identities to fraudulently obtain $2.1 million in unemployment insurance benefits from multiple states and to traffic in methamphetamine.

Read more here.

The DOJ’s COVID-19 Fraud Enforcement Task Force has made significant strides in combating this fraud, with over 3,500 defendants criminally charged with more than $1.4 billion in fraudulently obtained CARES Act funds seized or forfeited and more than 400 civil settlements and judgments.

However, the sheer magnitude of the fraud indicates that much work remains to be done.

[...]

False positive cases nearly cost us our society. Hospitals cashed in, to the tune of $250,000 dollars per COVID-19 hospitalization - far more than needed.

In March 2023, The New York Times published this image showing that $483 billion of government aid had been spent to bail out big medicine. Right off the bat, we see $64 billion was wasted on vaccines that do not prevent transmission and only look like they reduce COVID-19 severity if you ignore COVID-19 cases for 8 weeks after the first exposure.

Given the shell-and-pea game of reimbursements, cost-sharing, Medicaid and Medicare and COBRA payments to healthcare providers totaled $125 Billion - on top of the $156 paid directly to healthcare providers for a grand total of $281 Billion.

There are about 920 thousand (corrected from million) hospital beds in the United States, and not all beds were used for COVID-19. According to NPR, only 1/5 of hospital beds were dedicated to COVID-19 beds. That means at least $1.5M were given to hospitals per COVID-19 hospital bed.

But that’s a pittance. According to the AHA, in March 2021, $1.9 Trillion were actually allocated to Big Medicine under a "Relief Reconciliation" scheme - basically a bail-out of nearly every aspect of Big Medicine… to make up for insufficient compensation to healthcare providers.

The AHA complained there was no relief in the Relief Reconciliation to healthcare providers… yet via indirect compensation, all hospital costs were clearly programmed for overcompensation.

According to this published report reported costs per patients, however, were at most $50,000 (and that's for ventilated patients). At the low-end costs were $14K per patient.

CDC estimates there have been 7.5 million COVID-19 hospitalizations. Given the $1.9 Trillion dollar bail-out, each hospitalization cost the US $250,000, at least five times and more frequently ten times the amount of money required.

Admittedly these are general analyses that oversimplify. Still, I’ve said since 2015 medicine for profit is an unsustainable model. Let’s not call bail-outs of big medicine “Relief Reconciliation”. They are bailouts of an unsustainable business.

Big Medicine is unsustainable at any scale - meaning if we all get sick more often, the problem will get larger.

[...]

The world has been counting on the intelligence community to call out anything untoward about the response to COVID. Of course, that won’t happen, because they’re the ones who planned it.

From an early date, commentators have noted that the response to COVID had all the look and feel of a coup attempt. The masks, the slogans, the symbols, the lies, the sudden inversion of long-cherished norms and values, the mindless acceptance of information from nefarious sources like the World Health Organization and China. Something was seriously off, and it all seemed so obvious.

Thus, one overarching question always lingered over the response to COVID. How were officials able to implement such destructive, totalitarian policies across the western world without intelligence authorities stepping in to stop them?

A detached review of the evidence leads to a chilling answer—though in hindsight, perhaps the only one that was ever really possible. Quite simply, the reason the western intelligence community never stepped in to stop this illiberalism is that virtually all the most illiberal aspects of the response to COVID lead directly back to the western intelligence community itself.

Reviewing the Evidence

[...]

[...]

The line between being overly cautious and just plain cruel has been crossed repeatedly. This is where we are today in what had previously been thought of as civilization:

• Hospitals across the country are removing unvaccinated organ transplant patients from waiting lists. Medical ethicists are fine with this, because the patients need to be protected from illnesses while their bodies accept the new organs, and they are prioritized based on their chances of survival. These “ethicists,” however, come off as vindictive, “othering” the unvaccinated in line with the narrative. Moving these patients lower on the list based on a risk they assume seems acceptable, dropping them altogether is not. It’s intentionally punitive and ghoulish. The decisions reinforce, as well, the naked fact that the vaccine mandates are authoritarian power plays.
• A Virginia hospital that refused to provide Ivermectin prescribed by a doctor to a dying COVID patient was found in contempt of court before it finally relented and allowed the drug to be administered. It was too late, though. The woman died five days after the judge’s ruling.
• At Georgetown University,​​ “fully vaccinated students are randomly tested for COVID each week,” the Daily Mail reported last month, “and even those who are asymptomatic are ordered to stay in a room in a designated building where they spend 10 days in confinement.”

[...]

Throughout wave after wave of COVID-19, a range of voices have called for reforming the way governments manage pandemics. From mixed messages to inequitable vaccine distribution, the global response to COVID-19 just hasn’t cut it. In particular, critics have highlighted the World Health Organization (WHO) as a primary target for reform efforts, and, by now, several groups inside and outside of the organization have begun developing proposals that range from reforming the WHO to developing whole new international forums specifically designed to prepare for and mount an effective pandemic response.

Last December, at a special meeting of the World Health Assembly, the governing body of the WHO, country representatives agreed to kick off reforms when they voted for negotiating an international agreement or pandemic treaty. With the vote, the conversation seemingly moved beyond simply reforming the WHO and towards the creation of a stand-alone legally binding instrument: a new international structure to address pandemics.

Pandemics could become more frequent in the years to come as the world grows even more interconnected, increased agricultural production leads to more contact between humans and animals with the potential for further spread of zoonotic diseases, and humans encroach further into wildlife areas. While an international pandemic organization sounds important in theory, organizations like the UN Security Council can’t necessarily solve the problems they were intended to solve. Creating a new pandemic response system will likely require years of difficult negotiations and could still result in a structure unable to forcefully respond to an outbreak, or an agreement supported by only some countries and perhaps not all of the key global leaders. By looking at the reform ideas that people and organizations have put forward, one can begin to see the contours of what a new global response system might look like.

[...]

Abstract

This analysis piece will attempt to examine some of the critical pandemic-related measures implemented in the United States from an immunological perspective and pinpoint caveats that should have been considered before their implementation. I also discuss alternative measures grounded in scientific data that were not thoroughly explored and likely could have helped fight the pandemic.

[...]

5. Alternative Measures to Vaccines to Fight the Pandemic

Bias towards vaccines as the single most crucial tool to fight the pandemic was evident from the beginning. However, these vaccines do not prevent infections and provide little protection from long COVID [72], and even if we succeeded in injecting the entire world population, we would have likely put an even stronger evolutionary pressure on the virus to mutate and evade the immune responses triggered by the vaccine. The best example of how non-sterilizing vaccines can lead to more pathogenic variants is the vaccine generated to fight Marek disease in poultry [73,74]. This caveat and those discussed above highlight the lack of a solid scientific rationale to focus on vaccines targeting a single viral component. We have been fighting influenza for decades. Influenza induces short- and long-term symptoms and kills people in a similar way to COVID, and the same target population is at risk [75,76,77,78,79,80,81]. We have a standard of care in place with influenza symptoms and other respiratory diseases, some of which could have been better used to treat COVID.

Efforts to repurpose drugs with high safety profiles could have been better supported and managed. Drug repurposing and developing novel therapeutics to treat COVID have been reviewed elsewhere [82]. Here, I will briefly discuss the efforts to repurpose two drugs, chloroquine (alone, or its hydroxy derivate, or combined with azithromycin) and remdesivir, to highlight possible concerns on how drugs become classified as effective by regulatory agencies. Chloroquine, hydroxychloroquine, and azithromycin are cheap and safe drugs taken by millions around the world daily for different inflammatory diseases and malaria. After some promising data on the use of these drugs to treat COVID [83], follow-up clinical trials failed to show their benefits in fighting COVID [84,85,86]; therefore, they were not implemented as the standard of care in Western countries. Chloroquine/hydroxychloroquine/azithromycin/ivermectin are still the primary go-to drugs in low-mortality-rate African countries to prevent and treat COVID [87,88,89,90]. Whether the low mortality rate in these countries is due to the use of these drugs or other factors, such as vaccination history [91,92,93], age, etc., remains to be determined [90]. In contrast, the previously untested remdesivir was fast-tracked and adopted as the standard of care despite opposing clinical trial outcomes [94]. One well-designed but maybe underpowered clinical trial did not reveal any statistically significant clinical benefits of remdesivir for treating severe COVID [95,96], and neither did the WHO Solidarity Trial [97]. In contrast, The National Institute of Allergy and Infectious Diseases (NIAID)-sponsored, somewhat controversial trial [98] found that remdesivir slightly reduced the duration of the disease (from 15 days to 11 days), though not mortality from COVID [99,100]. However, the already questionable benefits of using remdesivir might be even further diminished by reports of kidney and liver toxicity [101].

The monoclonal antibody therapy targeting the SARS-CoV-2 spike protein from Regeneron and others became available early in the pandemic. It was shown to be highly effective in preventing the development of severe illnesses and hospitalization without any significant side effects. This treatment option, which can now be easily administered subcutaneously [102], could likely have been made available to anyone who needed it for a fraction of the total vaccine costs.

Early research showed that patients with severe COVID had low levels of vitamin D [103,104,105]. People with dark skin need more sunlight than people of Northern European ancestry to generate similar amounts of vitamin D, and they are disproportionally affected by COVID [106,107,108]. Therefore, simple lifestyle adjustments that involve nutrition, exercise, and supplements should probably have been implemented as a preventative measure against COVID. These measures would likely also constitute a long-term general solution for achieving a much healthier population that is more resistant to infections and chronic diseases.

[...]

7. Layman’s Summary

The virus fatality rate did not support lockdowns, blanket restrictive measures, and non-selective mass vaccinations. There was no solid scientific rationale to adopt the untested mRNA-LNP platform over other well-established vaccine formulations to fight COVID. Scientists, experts, government officials, the media, and scientific journals, all contributed to suppressing alternative ideas on how to manage the pandemic. Some of these groups are still promoting the scientifically debunked idea that the present vaccines protect you from catching COVID and becoming sick [116], and that this is a pandemic of the unvaccinated [117]. Unfortunately, the virus is likely here to stay in one form or another, and we must learn to live with it. How effective the lockdowns and other restrictive measures were in reducing COVID deaths are still a matter of debate [118,119,120,121], but we likely lost, or we will lose a lot more people, from the direct and indirect effects of these measures. The excess of global deaths is often exclusively attributed to COVID [122]. However, these reports fail to factor in the direct and indirect effects of COVID-related restrictions. Many people died because they did not have access to healthcare during this period (they were afraid of going to the hospitals, or the hospitals did not accept them). Furthermore, a significant increase in suicide rates, drug and alcohol abuse, domestic violence, obesity, economic hardships, vaccination-related events, etc., likely contributed to excess deaths. If the vaccines do not prevent infections and spread, it is time to stop coercing people to get vaccinated, vilifying unvaccinated people, and giving extra perks to the vaccinated. It is neither feasible nor economically sustainable to “vaccinate” everyone every few months or perform continuous testing, and more importantly, there is no scientific rationale for doing so. We must focus our resources on the vulnerable population and provide them with efficient treatment options and possible preventative steps in the form of lifestyle changes, supplements, and effective, long-lasting, safe, and affordable vaccines.

[...]

[...]

Evidence-Based Medicine

There is perhaps no bigger plausibility sham today than “evidence-based medicine” (EBM). This term was coined by Gordon Guyatt in 1990, after his first attempt, “Scientific Medicine,” failed to gain acceptance the previous year. As a university epidemiologist in 1991, I was insulted by the hubris and ignorance in the use of this term, EBM, as if medical evidence were somehow “unscientific” until proclaimed a new discipline with new rules for evidence. I was not alone in criticism of EBM (Sackett et al., 1996), though much of that negative response seems to have been based on loss of narrative control rather than on objective review of what medical research had actually accomplished without “EBM.”

[...]

Conclusions

Many other instances of plausible scientific claptrap or bad science have occurred during the Covid-19 pandemic. As was seen with the retracted Surgisphere papers, medical journals routinely and uncritically publish this nonsense as long as conclusions align with government policies. This body of fake knowledge has been promulgated at the highest levels, by the NSC, FDA, CDC, NIH, WHO, Wellcome Trust, AMA, medical specialty boards, state and local public health agencies, multinational pharma companies and other organizations around the world that have violated their responsibilities to the public or have purposely chosen not to understand the fake science. 

The US Senate recently voted, for the third time, to end the Covid-19 state of emergency, yet President Biden stated that he would veto the measure because of “fear” of recurring case numbers. My colleagues and I argued almost a year ago that the pandemic emergency was over (Risch et al., 2022), yet the spurious reliance on case counts to justify suppression of human rights under the cover of “emergency” continues unabated.

Massive censorship by the traditional media and much of social media has blocked most public discussion of this bad and fake science. Censorship is the tool of the undefendable, since valid science inherently defends itself. Until the public begins to understand the difference between plausibility and science and how large the effort has been to mass-produce science “product” that looks like science but is not, the process will continue and leaders seeking authoritarian power will continue to rely on it for fake justification.

Trend Over Last Few Years Indicates Fear of the Truth Amongst Vaccine Promoters

[...]

Hotez is now joined by Tedros at the WHO and Fauci (retired NIH) in promulgating the term anti-science as a pejorative and insulting way of positioning clinical scientists who are studying the epidemiology, pathophysiology, and clinical consequences of COVID-19 vaccine injuries, disabilities, and deaths. Yes, the study of what COVID-19 vaccines do to the human body is “science” and it is insulting to hear the term “anti-science” thrown out as a blocking tool in order to discount any side effects of vaccination.

Tedros went so far as to say those studying vaccine injuries and who wisely chose to defer on vaccination themselves are “killing machines.” This unhinged hyperbole is symptomatic of a psychotic break in those who who have been the vanguard of the imploding worldwide narrative supporting mass vaccination.

I summarized these comments and pivoted on television to the opportunities that Drs Fauci, Walensky, Jha, Murthy, and several others had on Jan 24 and Dec 7, 2022, to attend US Senate Hearings and listen to COVID-19 experts and have an interchange on the “science” of what we have learned. Instead none of them showed up and now are painting themselves with the term “anti-science”. This regression can only lead to greater loss of credibility and dissolution of the crumbling false narrative “safe and effective.”

[...]

Abstract

Background: The COVID-19 period highlights a huge problem that has been developing for decades, the control of science by industry. In the 1950s, the tobacco industry set the example, which the pharmaceutical industry followed. Since then, the latter has been regularly condemned for illegal marketing, misrepresentation of experimental results, dissimulation of information about the dangers of drugs, and considered as criminal. Therefore, this study was conducted to show that knowledge is powerfully manipulated by harmful corporations, whose goals are: 1/financial; 2/to suppress our ability to make choices to acquire global control of public health.

Methods: Pharmaceutical industry techniques for manipulating science and COVID-19 reporting were reviewed. Several sources of official documents were used: PubMed; National Institutes of Health resources; pharmaceutical companies; policy documents; national newspapers and news agencies; and books by prominent professionals (scientific and legal). A few studies have not been published in peer-reviewed journals; however, they have been conducted by reputable scientists in their respective fields.

Results: Since the beginning of COVID-19, we can list the following methods of information manipulation which have been used: falsified clinical trials and inaccessible data; fake or conflict-of-interest studies; concealment of vaccines' short-term side effects and total lack of knowledge of the long-term effects of COVID-19 vaccination; doubtful composition of vaccines; inadequate testing methods; governments and international organizations under conflicts of interest; bribed physicians; the denigration of renowned scientists; the banning of all alternative effective treatments; unscientific and liberticidal social methods; government use of behavior modification and social engineering techniques to impose confinements, masks, and vaccine acceptance; scientific censorship by the media.

Conclusion: By supporting and selecting only the one side of science information while suppressing alternative viewpoints, and with obvious conflicts of interest revealed by this study, governments and the media constantly disinform the public. Consequently, the unscientifically validated vaccination laws, originating from industry-controlled medical science, led to the adoption of social measures for the supposed protection of the public but which became serious threats to the health and freedoms of the population.

Republicans in the New Hampshire House united this week to pass multiple bills dealing with COVID-19, with a focus on prioritizing individual rights and limiting the authority of entities to compel adherence to public health policies.

The action by the House moves the debate over COVID policy to the state Senate, which has so far heard far fewer bills related to the pandemic than the House. In fact, questions of masking, vaccines, and the reach of government have been on the front burner for House lawmakers all year.

[...]

The most high-profile bill, sponsored by House Speaker Sherman Packard, would bar the state from enforcing federal vaccine mandates. Before that proposal was voted through along near party lines. Rep. Mark Pearson of Hampstead, who is chair of the House Health and Human Services Committee, asked colleagues to recognize there is a long tradition of states bucking federal laws.

“In the 19th century, some northern states passed individual liberty laws, which made it illegal for citizens of their states to help enforce the Fugitive Slave Act,” Pearson said.

The House also voted to outlaw mask mandates in public schools (H.B. 1131), and to give the Legislature final say over any decision by the state’s health commissioner to add a vaccine to the list of required inoculations for children (H.B. 1379).

[...]

We need to be careful to avoid declaring victory over Covid tyranny. You may have thought that with the worldwide protests against mask mandates and lockdowns, and the deaths attributable to the vaccine poisons, our enemies would at least give us a break. But of course they’re not. They are planning a new fake “Covid wave” with more lockdowns, mask mandates, and deadly vaccines. In short, global tyranny.

Information is coming in all the time about the criminal folly of brain-dead Biden and “Dr. Death” Fauci’s policy. For example, a renowned oncologist, Dr. Angus Dalgleish, wrote an open letter to a leading British medical journal warning that the vaccines cause cancer: “Dr. Angus Dalgleish, a renowned oncologist practising in the UK, recently wrote an open letter to the editor-in-chief of the medical journal The BMJ, urging the journal that harmful effects of Covid injections be ‘aired and debated immediately’ because cancers and other diseases are rapidly progressing among ‘boosted’ people.

Dr. Dalgleish is a Professor of Oncology at St George’s, University of London. His letter to Dr. Kamran Abbasi, the Editor in Chief of the BMJ, was written in support of a colleague’s plea to Dr. Abbasi that the BMJ make valid informed consent for Covid vaccination a priority topic.

Read Prof. Dalgleish’s letter below:

Dear Kamran Abbasi,

Covid no longer needs a vaccine programme given the average age of death of Covid in the UK is 82 and from all other causes is 81 and falling.

The link with clots, myocarditis, heart attacks and strokes is now well accepted, as is the link with myelitis and neuropathy. (We predicted these side effects in our June 2020 QRBD article Sorensen et al. 2020, as the blast analysis revealed 79% homologies to human epitopes, especially PF4 and myelin.)

However, there is now another reason to halt all vaccine programmes. As a practising oncologist I am seeing people with stable disease rapidly progress after being forced to have a booster, usually so they can travel.

Even within my own personal contacts I am seeing B cell-based disease after the boosters. They describe being distinctly unwell a few days to weeks after the booster – one developing leukaemia, two work colleagues Non-Hodgkin’s lymphoma, and an old friend who has felt like he has had Long Covid since receiving his booster and who, after getting severe bone pain, has been diagnosed as having multiple metastases from a rare B cell disorder.

I am experienced enough to know that these are not the coincidental anecdotes that many suggest, especially as the same pattern is being seen in Germany, Australia and the USA.

The reports of innate immune suppression after mRNA for several weeks would fit, as all these patients to date have melanoma or B cell based cancers, which are very susceptible to immune control – and that is before the reports of suppressor gene suppression by mRNA in laboratory experiments.

This must be aired and debated immediately.

[...]

The Lancet Commission on the coronavirus pandemic has delivered a harsh verdict on how the world responded — it was “a massive global failure,” the prestigious journal declared. Governments were too slow and cautious, faced deep public mistrust, were undermined by misinformation and failed to serve the most vulnerable. “The result was millions of preventable deaths,” the Lancet said. This sorry record must provide impetus to do better in the future.

The Lancet convened 28 experts under Columbia University’s Jeffrey Sachs for a two-year examination of pandemic preparedness, response and recovery, delving into public health, virology, social policy, economics, finance and geopolitics. The report is but one of several worthy efforts to draw lessons from the gravest public health disaster in a century. The authoritative new findings deserve attention, though we wish Congress and the White House had ordered a comprehensive, 9/11 Commission-like national panel in the United States. They did not.

A major lesson is that when a highly infectious disease breaks out in a vulnerable population, rapid response is essential, and even more so when many infections are asymptomatic, as was the case with covid-19. A single new case became thousands within a month. “The ability of the public health system to identify cases, trace contacts, and isolate infected individuals can be overwhelmed in just a few weeks of uncontrolled community transmission,” the report says. That’s what happened, over and over. “National responses were often improvisational, occasionally bordering on the absurd,” the commission states. “Several national leaders made highly irresponsible statements in the first few months of the outbreak, neglecting scientific evidence and needlessly risking lives with a view to keeping the economy open.” Governments “showed themselves to be untrustworthy and ineffective,” and “rancor among the major powers” then “gravely weakened the capacity of international institutions” to respond, especially the World Health Organization, which comes in for sharp criticism for repeatedly erring “on the side of reserve rather than boldness.” The panel calls for strengthening the WHO and giving it stronger powers and more solid financing.

[...]

[...]

Here are the 10 biggest falsehoods—known for years to be false, not recently learned or proven to be so—promoted by America's public health leaders, elected and unelected officials, and now-discredited academics:

1. SARS-CoV-2 coronavirus has a far higher fatality rate than the flu by several orders of magnitude.

2. Everyone is at significant risk to die from this virus.

3. No one has any immunological protection, because this virus is completely new.

4. Asymptomatic people are major drivers of the spread.

5. Locking down—closing schools and businesses, confining people to their homes, stopping non-COVID medical care, and eliminating travel—will stop or eliminate the virus.

6. Masks will protect everyone and stop the spread.

7. The virus is known to be naturally occurring, and claiming it originated in a lab is a conspiracy theory.

8. Teachers are at especially high risk.

9. COVID vaccines stop the spread of the infection.

10. Immune protection only comes from a vaccine.

None of us are so naïve as to expect a direct apology from critics at my employer, Stanford University, or in government, academic public health, and the media. But to ensure that this never happens again, government leaders, power-driven officials, and influential academics and advisors often harboring conflicts of interest must be held accountable. Personally, I remain highly skeptical that any government investigation or commission can avoid politicization. Regardless of their intention, all such government-run inquiries will at least be perceived as politically motivated and their conclusions will be rejected outright by many. Those investigations must proceed, though, if only to seek the truth, to teach our children that truth matters, and to remember G.K. Chesterton's critical lesson that "Right is right, even if nobody does it. Wrong is wrong, even if everybody is wrong about it."

The last three and a half years have been times of enormous upheaval. It has affected politics, economics, culture, media, and technology. It’s not just about the spreading of economic, cultural, and demographic decay. Millions and billions of lives have been wrecked, to be sure, but there is also a big impact on the way we see the world around us. 

What we once trusted, we now doubt and even disbelieve as a matter of new habit. The simple categories of understanding that we once deployed to make sense of the world have been tested, challenged, and even overthrown. Old forms of ideological commitments have opened their way to new. This particularly pertains to intellectuals. 

Or should in any case. If you have not shifted your thinking in some respect over these years, you are either a prophet, asleep, or in denial. The way social media works today, influencers are reluctant to admit it lest risk their followings built out of a prior cultural landscape. This is really too bad. There is nothing wrong with changing, adapting, migrating, and calling out truth even if that contradicts what you once said or how you used to believe.

There is no need to change your principles or ideals. What should change in light of evidence is your evaluation of the problems and threats, your outlook on the relative priorities of focus, your perceptions of the functionality of institutional structures, your awareness of issues and concerns about which you had limited prior knowledge, your political and cultural allegiances, and so on. 

These days, this intellectual migration seems mainly to have affected the left. Nearly daily I find myself having the same conversations with people in person, on the phone, or online. It is from an Obama voter and someone with traditionally “liberal” allegiances. 

The Covid era utterly shocked them in what they discovered about their own tribe. They aren’t liberal at all. They supported universal quarantine, forced face coverings, and then mandatory jabs pushed by a tax-funded corporate monopoly. Concerns about human rights, civil liberties, and the common good suddenly evaporated. Then of course they turned to the most blunt instrument of all: censorship. 

The trauma felt by principled people who imagined themselves to be “on the left” is palpable. But the same is true of people “on the right” who were aghast to observe that it was Trump and his administration that greenlighted lockdowns, spent many trillions forcing Covid compliance, and then threw public monies at Big Pharma to rush a shot by bypassing all standards of necessity, safety, and effectiveness. 

The promise to “make America great again” ended in wreckage coast-to-coast. For Trump partisans, this realization that it all happened under their hero is hard to take, a triangulating rope-a-dope. Even more strangely, it was the “never Trumpers” on the right who most strongly supported lockdowns, masking, and shot mandates.

The libertarians are another story entirely, one that nearly surpasses understanding. Among the higher echelons of this faction in academia and think tanks, the silence from the start and even years later was truly deafening. Instead of standing up to totalitarianism, as the whole of the intellectual tradition had prepared them to do, they deployed their clever heuristics to justify outrages against core freedoms, even the freedom to associate. 

So, yes, observing one’s own tribe collapse into craven careerism and coercion is disorienting. But the problem goes even deeper. The most striking alliance of our time has been to observe the lockstep of the elites in government, media, tech, and academia. The reality blows apart the traditional binary of public vs private that has dominated ideological discussion for centuries. 

[...]

[...]

Skepticism and Rejection of Smallpox Vaccination

Initially Jenner’s claims (first published in 1798) were met with much skepticism, as many physicians had observed patients develop cowpox and subsequently smallpox, and others questioned the basic validity of his studies (one physician who tested 3 children with Jenner’s vaccine found all 3 subsequently developed smallpox after inoculation, with similar results obtained by other physicians). Nonetheless, the practice gradually caught on, became a larger share of physician income, became more and more popular within the medical field, and over the next hundred years, the number of dissenting physicians gradually diminished. However, what is relatively unknown now is that many did speak out, and published literature with data showing serious issues with the vaccine.

[...]

Mandatory Smallpox Vaccination

As it became clear that the smallpox vaccine was unable to prevent disease as initially promised, the medical profession moved the goal posts from lifelong “perfect” immunity to “milder disease” to justify vaccination, a tactic that has since repeated with other vaccination campaigns.

Mr. Henry May, writing to the Birmingham Medical Review, in January, 1874 reported that deaths as a result of vaccination were often not reported because of an allegiance to the practice. Often a vaccinated person was recorded as having died from another condition such as chicken pox or erroneously listed as unvaccinated. 

This corruption of the vital statistics creates many challenges in assessing the efficacy of immunization, and is also why many authors argue no metric can be used to assess COVID-19 immunizations except total number of deaths (independent of cause) as this cannot be fudged. Of note, a different significant overlap exists with the early Polio campaigns (also detailed within the book), where “Polio” diagnostic criteria was repeatedly adjusted to meet the political need for Polio cases.

Governments responded to this skepticism by progressively using more and more force to mandate vaccination. Vaccination was made compulsory in England in 1853, with stricter laws passed in 1867. In the United States, Massachusetts created a set of comprehensive vaccination laws in 1855 (which created the Supreme Court case Jacobson v. Massachusetts a case that is frequently cited about state enforced vaccination). Lemuel Shattuck emphasized the need for vaccination and pushed for house-to-house vaccination to be enforced by the authority of the City of Boston in an 1856 report, also noting ““The City has already provided that no unvaccinated child shall be admitted into the public schools.”

[...]

A situation emerged I term the vaccine positive feedback cycle. Keep in mind that most systems in nature are instead negative feedback systems. In these, when something occurs, it self-corrects the system and turns it off rather than accelerating it, as occurs in a positive feedback system.

The cycle is as follows:

A concerning disease exists

↓

Immunization is cited as a potential solution to the problem

↓

A preliminary immunization campaign is conducted and makes the problem worse

↓

As the problem is now worse, the need for immunizations to address it increases and another campaign is conducted

↓

This makes the problem worse

↓

This increases the need for more aggressive measures to increase immunization

↓

This makes the problem worse and further perpetuates the cycle, before long leading to very questionable governmental policies designed to force unwilling parties to vaccinate. 

The underlying drivers of this process seem to be an unquestionable faith in vaccination, a conviction dating back to the days of smallpox, that vaccinating an ever increasing proportion of the population through vaccination can end epidemics (now termed herd immunity), and the government having limited options to address the issue besides immunizations and governmental force.

[...]

Effects of Mandatory Smallpox Vaccination

In accordance the positive feedback cycle, these results were found everywhere. Within the United States, as smallpox worsened in Boston, in 1855, the government enacted strict enforcement of vaccination. It was followed by the epidemics of 1859-1860, 1864-1865, 1867 (these were all similar in size to earlier epidemics), and then infamous 1872-1873 epidemic which dwarfed all previous epidemics (proving fatal to 1040 persons, at a rate of 280 deaths per 100,000 people).

By the end of 1868, more than 95 percent of the inhabitants of Chicago had been vaccinated. After the Great Fire of 1871 (it leveled the city), strict vaccine laws were passed, and vaccination was made a condition of receiving relief supplies. Chicago was then hit with a devastating smallpox epidemic in 1872 where over 2000 persons contracted smallpox, with over 25% dying, and the fatality rate among children under 5 being the highest ever recorded.

[...]

Joining me today is Professor Richard Werner, here to discuss COVID-19 from an economic perspective, and the role central banks are playing in this rapidly shifting financial and societal landscape.

• The World Bank bonds offer investors high interest payments in return for taking on the risk of losing a certain amount or all of their money if pandemics occur. That includes the current coronavirus pandemic.
• But prices of those bonds have plunged, as investors flee with the number of cases surging.
• According to ratings agency DBRS Morningstar, investors who hold the riskier of the two bonds could be losing their entire principal amount soon, with the firm saying that the price should have dropped more than 80%.

GDP levels had already recovered to pre-pandemic levels when coercive vaccine mandates were introduced

The government measures in response to the declaration of the pandemic caused a drop in the level of economic activity as measured by the GDP (gross domestic product). By drawing trendlines over the GDP data we can estimate what the economic levels would have been without the government covid-19 measures. Conceptually it looks like the following chart. 

[...]

The pandemic health and economic crises have contributed to a further widening of long-standing economic, racial, and gender divides.

Wealth and Income Inequality and Covid-19

Racial Inequality and Covid-19

Inequality Across Gender Diversity and Covid-19

Covid-19 and Inequality in the Care Economy

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As ordinary people around the world suffer from the health and economic impacts of the pandemic, billionaires have actually seen their fortunes expand. According to Institute for Policy Studies analysis of Forbes data, the combined wealth of all U.S. billionaires increased by $2.071 trillion (70.3 percent) between March 18, 2020 and Ocobter 15, 2021, from approximately $2.947 trillion to $5.019 trillion. Of the more than 700 U.S. billionaires, the richest five (Jeff Bezos, Bill Gates, Mark Zuckerberg, Larry Page, and Elon Musk) saw an 123 percent increase in their combined wealth during this period, from $349 billion to $779 billion. We will be regularly updating this analysis here.

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COVID-19 is dramatically changing the economic landscape. Some industries are faring well while others are being devastated by the pandemic. Businesses are rapidly adapting to the demands and peculiarities of living within the constraints of a pandemic. Of particular concern to me is the plight of small businesses. In many ways, small businesses are the lifeblood of the American economy. Indeed, before COVID-19, various studies found that small businesses accounted for about 50% of private-sector jobs. Moreover, Americans highly value their right to start a small business – be it a local restaurant, a small retail shop, or an online business. 

But small businesses historically have been adversely impacted by recessions in part because many small businesses operate on limited cash flow. This begs the question: how are small businesses enduring this now prolonged impact of COVID-19?

When COVID-19 began in the spring and many states shut down or substantially reduced various business services, it was clear that small businesses were skeptical they could survive a prolonged pandemic. For example, in an April 2020 survey of 5,850 small businesses across the country, Main Street America found that 75% of respondents reported that their business revenues had declined by more than half. And 66% of respondents predicted their business would be at risk of closing if the economic impact of the pandemic continued for 3 to 5 months.

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Moreover, certain industries and certain types of small businesses have been particularly hard hit by the pandemic. Studies have found that small businesses in certain geographic areas have been strongly hit by the economic impact of the pandemic, including those in more densely populated cities. And most studies have found that minority-owned small businesses have been particularly hard hit by COVID-19. In addition, studies estimate that many of the hardest-hit industries will not likely return to the levels of business that existed pre-COVID-19 for at least 5 years. This includes industries which involve a lot of small businesses such as restaurants, hospitality, retail and education. Finally, new business start-ups have also fallen dramatically since the spring – a trend that needs to substantially change for our economy to recover from this pandemic!

Despite all these challenges, it appears that small businesses are rapidly adapting to the new normal of running a business amidst a pandemic. Locally-owned restaurants have added curbside pickup and are gradually expanding the to-go portion of their business. Local retailers are also now frequently offering curbside pickup in addition to adjusting their hours, limiting the number of customers, and even offering special hours for their most vulnerable customers. Various small businesses are substantially expanding their online offerings. Small business manufacturers are adjusting their work environments to allow for appropriate social distancing through the creation of manufacturing pods. Small businesses generally are greatly expanding their work-at-home options and related support capabilities. And at least some new small business opportunities are being created amidst this pandemic – note the advent of COVID-19 disinfection services!

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About this Research Topic

Market-driven economies, privatization, and the medicalization of health, amongst other factors, have all been shaped by, and are shaping corporate behaviors. This sits alongside the rapid growth in size and internationalisation of the very largest corporations, with the revenues of companies like Walmart, Volkswagen and Amazon now exceeding that of entire countries.
The 'industrial epidemic' hits vulnerable populations the hardest and is a direct consequence of corporate practices. These practices include the production and sale of unhealthy commodities, tax evasion, child labor, marketing to children, the distortion of science, and lobbying. Collectively, they have been described as 'commercial determinants of health'.
The current COVID-19 pandemic has seen many larger corporations increase their revenues, while they have also been responsible for growing inequities and negative impacts on population and planetary health.
The social and economic impacts of the COVID-19 pandemic are vast, yet little is known about corporate political practices and the action of corporate power during the pandemic, and how these are shaping population and planetary health. There is evidence that alcohol and tobacco companies lobbied for carcinogenic products to be listed as essential commodities during the first lockdown period. Tobacco companies have used the pandemic to polish their bad reputation, by investing in vaccines development and in community responses. Food companies have used the pandemic to put a health halo on ultra-processed food products. Some have called this `disaster capitalism', where corporations use crises to strengthen their market position and social power.
For this Research Topic, we are interested in exploring the impacts of corporate power and political practices in response to the COVID-19 pandemic on public and planetary health. We have no restriction on the type of industry that is discussed. Manuscripts must provide scientific knowledge and evidence relevant to public health policy, research or/and practice.
We are interested in receiving Original Research articles, Systematic Reviews, Reviews, Policy and Practice Reviews, and Community Case Studies. Submissions could cover but are not limited to the following topics:
§ Corporate structural, instrumental and discursive power and the COVID-19 pandemic, in relation to public and/or planetary health
§ Corporate political practices and their impacts on public and/or planetary health during the COVID-19 pandemic, including the influence on science, policy and practice;
§ Ethical issues in public health related to corporations and their responses to the COVID-19 pandemic;
Conflicts of interest in public health during the COVID-19 pandemic.
Special note: We will not accept manuscripts reporting on research that is funded by the tobacco, alcohol, food, gambling, arm, oil, pharmaceutical, and other health-harming industries and third parties affiliated with them, or from authors who have previously worked for or with them. All authors are asked to declare their current or previous interactions with these industries when they exist, and any interaction they had with any other industry(ies) described in their manuscript. We will reject manuscripts where there are clear conflicts of interest.

The Federal Reserve has moved with unprecedented force and speed to pump huge amounts of cash into the financial system to ease disruptions that have escalated since the viral outbreak

WASHINGTON -- The Federal Reserve moved with unprecedented force and speed Friday to pump huge amounts of cash into the financial system to ease disruptions that have escalated since the viral outbreak.

The New York Federal Reserve Bank said it will offer $1 trillion of overnight loans a day through the end of this month to large banks. That is in addition to $1 trillion in 14-day loans it is offering every week. Banks, so far, have not borrowed nearly as much as the New York Fed is offering, and the loans are quickly repaid. None of the funding is from taxpayer dollars. Wall Street analysts say the huge number is intended to calm markets by demonstrating that the Fed's ability to lend short-term is nearly unlimited.

The Fed is also buying Treasury bonds at a furious pace, and will soon run through the $500 billion in purchases it announced on Sunday. It is also accelerating its purchases of mortgage-backed securities. Most analysts expect they will buy more.

“The Fed has just worked with unprecedented speed,” said Steven Friedman, a former economist at the New York Fed and senior macroeconomist at MacKay Shields, an asset manager. "I think there will be no hesitation on their part about buying as many Treasuries and mortgage-backed securities as necessary."

All the Fed's emergency steps are intended to pump cash into a financial system that has seen a spike in demand for dollars as investors unload Treasuries, municipal bonds, and other securities. With the economy likely in recession, banks, money market funds and other institutional investors are increasingly wary about holding securities that may lose value.

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WASHINGTON (AP) — The Federal Reserve moved with unprecedented force and speed Friday to pump huge amounts of cash into the financial system to ease disruptions that have escalated since the viral outbreak.

The New York Federal Reserve Bank said it will offer $1 trillion of overnight loans a day through the end of this month to large banks. That is in addition to $1 trillion in 14-day loans it is offering every week. Banks, so far, have not borrowed nearly as much as the New York Fed is offering, and the loans are quickly repaid. None of the funding is from taxpayer dollars. Wall Street analysts say the huge number is intended to calm markets by demonstrating that the Fed’s ability to lend short-term is nearly unlimited.

The Fed is also buying Treasury bonds at a furious pace, and will soon run through the $500 billion in purchases it announced on Sunday. It is also accelerating its purchases of mortgage-backed securities. Most analysts expect they will buy more.

“The Fed has just worked with unprecedented speed,” said Steven Friedman, a former economist at the New York Fed and senior macroeconomist at MacKay Shields, an asset manager. “I think there will be no hesitation on their part about buying as many Treasuries and mortgage-backed securities as necessary.”

All the Fed’s emergency steps are intended to pump cash into a financial system that has seen a spike in demand for dollars as investors unload Treasuries, municipal bonds, and other securities. With the economy likely in recession, banks, money market funds and other institutional investors are increasingly wary about holding securities that may lose value.

Companies will see revenue and earnings plunge, while local and state governments are likely to see lower tax revenue. That makes it harder for them to borrow.

“There is a growing certainty that we’re facing an economic contraction, so it’s natural for investors to become more concerned about risk,” Friedman said. “The Fed is trying to play the role of shock absorber.”

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Topline: As stocks headed for their worst day since 1987’s Black Monday Crash, the Federal Reserve announced further measures to prop up liquidity including a potential injection of more than $1.5 trillion into the market; stocks responded immediately, cutting losses in half on the announcement, before dropping back down 8%. 

• The Fed said it will ramp up its overnight funding operations—buying “repos,” or repurchase agreements—by $1.5 trillion over the next two days.
• “These changes are being made to address highly unusual disruptions in Treasury financing markets associated with the coronavirus outbreak,” the New York Fed said in a statement on Thursday afternoon. 
• The Fed also widened the range for its reserve management purchases—which had previously been restricted to short-term Treasury bills—to include other types of financial instruments. 
• The moves are designed to preserve liquidity in the market; in other words, the Fed wants to prevent “freezes” and make sure buyers and sellers still have the ability to trade. 
• It’s the third time in four days the New York Fed has announced that it will bulk up lending in the repo market: on Tuesday, it announced an injection of $50 billion, and it added another $25 billion on Wednesday. 
• Stocks initially pared back nearly half their losses on the announcement, but within the hour had dropped back close to their previous daily lows; at 2:00 p.m. EST on Thursday, the Dow Jones Industrial Average was down 8%. 

Key background: Stocks rallied on Tuesday this week after President Trump promised to introduce an economic stimulus package to address the crisis, then dropped again on Wednesday when details about that plan were slow to emerge. European stocks cratered on Thursday morning after President Trump announced that he would ban travel to the U.S. from Europe for 30 days. The Fed’s actions this week have been focused on the repo market, where it lends financial institutions short term money overnight so they have enough cash to cover their operations throughout the day. Repo is short for “repurchase agreement"; in these transactions, the Fed buys securities from a seller (a bank, or hedge fund, for example) who agrees to repurchase them later on with a bit of interest. This helps the Fed inject more cash into the banking system.