EMERGENCY ALERT!

BRITISH GOVERNMENT WARNS 

COVID VACCINE MAY KILL 2.6 BILLION PEOPLE ACROSS THE PLANET

By

Søren Nielsen

2021

We have watched SARS-CoV-2 develop for 18 months and have some idea of its trajectory. 

The Delta variant is the prime example of strains succeeding each other, becoming progressively worse in waves of infection. 

According to a recent report from the Scientific Advisory Group for Emergencies (SAGE) in the United Kingdom, the virus is very likely to evolve into a still more dangerous form. 

We must be prepared for this outcome, for we are already behind the curve as SARS-CoV-2 is outpacing our response.

Intended for reference by Prime Minister Boris Johnson and key public health decision-makers, the report compiled by leading physicians, scientists, and epidemiologists outlines what is known about viral evolution presents scenarios we are likely to encounter in the coming months and years as the Delta variant continues to evolve into something even more dangerous. 

The report assigns probabilities for each scenario and recommends strategies to limit the damage and control the pandemic.

The report outlines four scenarios: 

Scenario one: The Delta variant mutates to a point of increased lethality. Under this scenario, the virus has the potential to kill between 10 and 35% of people infected, as did SARS-CoV and MERS-CoV, up from the 1 to 2% lethality, characteristic of the current strains.

Scenario two: The Delta variant mutates to evade vaccines.

Scenario three: The Delta variant mutates to a point of multi-drug resistance, challenging antiviral treatments designed to prevent and treat disease. 

Scenario four: The Delta variant mutates to become less harmful, similar to the four coronaviruses circulating today, such as the common cold.

Before dissecting these scenarios, it is important to recognize the basis of their conclusions. 

The report is cognizant of the behavioral patterns of viruses and coronaviruses in particular. 

They can alter their genetic structures by mutation and recombination, leading to substantial changes in fundamental characteristics, including replication rate, transmission efficiency, and pathogenesis.

In what follows, we provide a detailed summary and analysis of each scenario.

Scenario One: Increased Lethality 

The SAGE report considers the development of strains with increased lethality a realistic possibility.

The Delta variant has driven a rise in cases to levels we have not observed in the United States since mid-February, and recent data shows a surge in deaths related to Delta variant infection in the UK, their highest rates since mid-March. 

The SAGE report highlights the possibility of recombination between two aggressive variants, resulting in a new, substantially more lethal and virulent virus. 

Specifically, the report highlights the possibility of an alpha and beta variant recombination. 

Were these variants to recombine, the variant could be comprised of the best of both worlds, forming a variant of dangerous transmission and immune evasion.

The report highlights another likely origin of a more pathogenic virus through the current advent of antigenic drift. 

Orf and structural proteins are particularly important in the suppression of host immune responses. 

Orf9b, for example, suppresses innate immunity by targeting mitochondria and the mitochondrial antiviral signaling protein (MAVS), TNF receptor-associated factor 3 (TRAF3), and TRAF6. 

In the alpha variant, a single amino acid mutation in the latter portion of the genome enabled the virus to replicate Orf9b mRNA to 80-fold greater amounts than in non-alpha variant samples.

As the report notes, the "likelihood of genotypic change in internal genes...is high." 

So long as infections continue, the virus will continue to mutate to better adapt to its host environment: us. 

If a single amino acid outside the S protein could enhance an immune suppression function by 80-fold, imagine the evolutionary capacity of dozens of other fine-tuned mutations down the line.

Scenario Two: Evading Vaccines

The SAGE report considers the possibility that the virus will develop into what I call "vaccine-busting variants" to be an almost certainty.

Influenza is an effective model for their concern. 

In addition to successive antigenic mutations that avoid immune suppression, a coronavirus has the evolutionary capability of antigenic shift, which involves substituting one or more genomic segments from a prevalent strain to an unrelated strain of animal origin. 

Such antigenic shifts of Influenza have occurred three times over the past century, each time giving rise to a new strain of flu, which evades existing prior immunity.

We note that a number of human and other animal retroviruses make use of the same ACE2 receptor as SARS-CoV-2, and given that hundreds of millions of people around the world have been and will be infected with SARS-CoV-2, it is highly likely that such a recombination event could take place.

At present, we are witnessing real-time antigenic drift, which could also result in "vaccine-busting variants." 

Each variant, as they arise, contains a series of point mutations in the exterior spike protein, which serve to reduce the potency of extant vaccines and monoclonal antibodies. 

Observations based on the annual recurrence of cold-causing coronaviruses indicate that the virus has nowhere near exhausted its capacity to reduce recognition by antibodies produced by previous infection or vaccine.

Scenario Three: Anti-Viral Drug Resistance

The SAGE report considers the possibility that the virus will develop antiviral drug resistance to be likely.

The development of potent small-molecule antiviral drugs has been slower than originally anticipated. 

A problem plaguing the development of antiviral drugs is a long asymptomatic period prior to the onset of symptoms. 

By the time symptoms typically appear, the concentration of the virus has rapidly dropped in infected people and further treatment by anti-viral drugs yields limited efficacy. 

There are two strategies to counter. 

One is much more vigorous, which is the early identification of the infected, contact tracing, and use of antiviral drugs for prophylaxis. 

That has been a successful approach with monoclonal antibodies. 

The Regeneron combination monoclonal antibody was recently approved by the United States for preventing infections in nursing homes and other congregate living settings.

Resistance to single and, in some cases, multiple monoclonal antibodies is already apparent. 

Many of the variants can no longer be neutralized by monoclonal antibodies that were produced early in the pandemic. 

Reports from separate laboratory studies show that single combinations of small molecule drugs also result in rapid adaptation and resistance. 

The lessons learned from successful treatment and prophylaxis of HIV show that combinations of antiviral drugs are critical for both the prevention and treatment of HIV infections. 

Combination treatment with two or more drugs dramatically reduces the possibility that the virus would rapidly develop resistance. 

Currently, there are more than 25 drugs, focusing on at least five or five to six different HIV targets that are used in combination.

It is likely that a successful program for chemoprevention and treatment of coronaviruses requires a similar large pharmacopeia to cope with the virus’s propensity for developing resistance. 

The report urges dramatically increased research on the development of antiviral drugs. 

The model could be the recent drug, Xofluza, which was developed to prevent household transmission and length of influenza, and has been shown to reduce infection duration by 80% when administered promptly post-exposure to active Influenza infection. 

Scenario Four: Decreased Virulence

The SAGE report considers the possibility that the virus will develop decreased virulence to be a realistic possibility, only in the long term.

It is possible, but by no means certain, that over time the virus could mutate through a form that is highly transmissible but far less lethal. 

This may have been the case for the four coronaviruses currently in circulation, although there is no hard evidence to support this speculation. 

The report mentions that it is unlikely that the virus will mutate to become less lethal in the near future. 

They suggest that if the virus does mutate to a less lethal form, such mutations may occur over a period of many years to many decades.

This report is not entirely pessimistic. 

It offers a number of different approaches; many of these involve additional research and vaccines which may produce better immune responses, capable of protection from many different viruses. 

The report also calls for major increases in fundamental and applied research of coronaviruses to fill in glaring gaps in our knowledge necessary to create new generations of vaccines and antiviral drugs. 

Finally, the report mentions that we are not helpless in the face of these viral changes. 

Human behavior is a driving factor in the spread of the virus. 

Behavior modifications including mask-wearing, isolation, lockdowns, contact tracing, all combined with vaccines and antiviral drugs—something I am calling "Multimodal Covid Control"—holds a prospect for effective management of the Covid-19 pandemic.

An Engineered Doomsday

It concerns recent avian influenza H5N1 research, in which scientists in the Netherlands and at the University of Wisconsin found that by passaging the virus in ferrets it could acquire aerosol transmissibility. 

Let’s determine if the scientific facts warrant the frightening title.

The editorial begins by rebuking the scientists who carried out the experiments on H5N1:

"…the research should never have been undertaken because the potential harm is so catastrophic and the potential benefits from studying the virus so speculative.…they created a virus that could kill tens or hundreds of millions of people if it escaped confinement or was stolen by terrorists. …the new virus…ought to be destroyed."

The intent of the experiments was not to create a doomsday virus, but to answer questions about why the H5N1 virus transmits well among birds but not humans. 

This experiment cannot of course be done in humans, so it was carried out in ferrets, a model for influenza. 

The results show that aerosol transmissibility in ferrets can be achieved with just five amino acid changes, with no reduction in the virulence of the virus. 

That result does not mean that the same amino acid changes would have the same effect in humans – it just tells us that achieving aerosol transmissibility in an animal model is relatively easy.

Whether tens or hundreds of millions of people would be killed depends on the ability of a virus to not only transmit among humans, but to retain virulence. 

There is no evidence that the ferret-passaged H5N1 virus has these properties. 

In the unlikely event that the virus somehow escaped and began to infect people, its spread could be controlled by vaccines (candidates are under development) and antivirals (existing neuraminidase inhibitors are active against influenza H5N1).

The heart of the H5N1 controversy is encapsulated by the next passage:

"Thus far the virus has infected close to 600 humans and killed more than half of them, a fatality rate that far exceeds the 2 percent rate in the 1918 influenza pandemic that killed as many as 100 million people."

This statement refers to the fact that nearly 60% of the 573 WHO-confirmed H5N1 cases have died. 

This death rate appears staggering until one considers how it is calculated. 

The WHO case definition for H5N1 influenza states that an individual must have a febrile respiratory illness, known exposure to H5N1 virus in the previous 7 days, and confirmation of infection by virus culture, polymerase chain reaction, or tests for antibodies. 

These conditions are highly unlikely to be fulfilled in rural populations where most H5N1 infections probably occur. 

The case fatality ratio can only be calculated by dividing the number of deaths by the total number of infections – and we do not know the latter number. 

Of ten large studies that have tested for H5N1 antibodies in rural populations, two were negative and 5 reported the presence of H5 antibodies in 0.2 – 5.6% of indiviudals. 

Much more work needs to be done to determine the actual fatality rate of influenza H5N1, but the WHO estimate is orders of magnitude too high.

Next the Editors weigh in on publication of the ferret results:

"The Erasmus team believes that more than 100 laboratories and perhaps 1,000 scientists around the world need to know the precise mutations to look for. That would spread the information far too widely. It should suffice to have a few of the most sophisticated laboratories do the analyses."

As I have argued before, limiting the dissemination of scientific information only serves to impede progress. 

It is impossible to predict which laboratory is going to do the breakthrough experiment, and picking "sophisticated" laboratories is meaningless.

Then the Editors argue that the research has no value:

"Defenders of the research in Rotterdam claim it will provide two major benefits for protecting global health. But it is highly uncertain, even improbable, that the virus would mutate in nature along the pathways prodded in a laboratory environment, so the benefit of looking for these five mutations seems marginal."

I would like to see the studies on which this statement is based. 

It is well known in virology that mutations selected in laboratory experiments can be been identified in nature. 

For example, the mutations identified in the H5N1 influenza viruses that transmit among ferrets have indeed been observed naturally in animals. 

The fact is that no particular viral mutation is improbable, given the enormity of  viral diversity in nature.

The Editors write that the results of the H5N1 studies do not help determine if existing antiviral drugs and vaccines would be effective:

"But genetic changes that affect transmissibility do not necessarily change the properties that make a virus susceptible to drugs or to the antibodies produced by a vaccine, so that approach may not yield much useful new information."

Two of the currently used drugs for controlling influenza, Tamiflu and Relenza, act by inhibiting the viral neuraminidase enzyme. 

Its function is to allow viruses to spread from cell to cell, and could very likely be involved in ferret transmission. 

If changes in this protein lead to aerosol transmission among ferrets, they could alter sensitivity to the drugs. 

Other changes in the H5N1 virus might alter its protein profile, making it less sensitive to currently proposed vaccines. 

These are only two of many reasons why studying this H5N1 virus would yield a great deal of useful information. 

As noted in A flu virus risk worth taking by Anthony Fauci, Gary Nabel, and Francis Collins in the Washington Post, 

“…new data provide valuable insights that can inform influenza preparedness and help delineate the principles of virus transmission between species.”

I think it is a good idea to have a public dialogue to understand the goals of influenza H5N1 research. 

But the discussion should be based on scientific fact, not doomsday scenarios.