Lab in Boston Made What Could Be A Super-Killer SARS-COV-2

Extreme Danger: This is Gain-of-Function Research on Steroids

I was in shock when a couple of my colleagues directed me to a pre-print article that was posted online on Friday October 14, 2022. Pre-prints are scientific papers that have not yet undergone peer review and they have not been published in a journal. In this case, these nuances are moot. What is far more important is the product that has been described, along with the disclosure of the recipe to make it.

You can find the pre-print article at this link.

Here is the full citation:

Title: “Role of spike in the pathogenic and antigenic behavior of SARS-CoV-2 BA.1 Omicron”

Authors: Da-Yuan Chen, Devin Kenney, Chue Vin Chin, Alexander H. Tavares, Nazimuddin Khan, Hasahn L. Conway, GuanQun Liu, Manish C. Choudhary, Hans P. Gertje, Aoife K. O’Connell, Darrell N. Kotton, Alexandra Herrmann, Armin Ensser, John H. Connor, Markus Bosmann, Jonathan Z. Li, Michaela U. Gack, Susan C. Baker, Robert N. Kirchdoerfer, Yachana Kataria, Nicholas A. Crossland, Florian Douam, Mohsan Saeed

bioRxiv 2022.10.13.512134

doi: https://doi.org/10.1101/2022.10.13.512134

The Purported Intent of the Research

The bulk of the research, and the most dangerous aspects, were conducted at Boston University in Massachusetts, USA. In a nutshell, the authors made a ‘chimeric’ version of the severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2), which is the causative agent of the coronavirus disease that was first identified in 2019 (COVID-19). A chimera is a combination of two different biological entities. For example, my academic institution’s mascot is a gryphon, which is a combination of a lion and an eagle…

In the case of the paper in question, they made a SARS-CoV-2 that was part Omicron variant (the spike protein) and part ‘ancestral’ variant (meaning it was a variant from earlier in the declared pandemic). Apparently, they were trying to figure out what role the spike protein has played in the ability of the Omicron variant to escape the far-from-sterilizing COVID-19 jab-induced immune responses, as well as its role in pathogenicity (how the virus causes disease).

Here it is in the authors’ words:

“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.”

I don’t care what the hypothesis of the study was. The results are nightmarish.

To the Point: A Potentially Deadly SARS-CoV-2 was Engineered

When the chimeric SARS-CoV-2 was tested in mice that express the same high-affinity viral entry receptor that people do, the authors dropped this bombshell…

“…while Omicron causes mild, non-fatal infection, the Omicron S-carrying virus inflicts severe disease with a mortality rate of 80%.”

This is a classic example of gain-of-function research.

It was gain-of-function research that resulted in SARS-CoV-2 in the first place. People like U.S. senator and physician Rand Paul have essentially proved this fact. Notably, while squirming under Senator Paul’s questioning, Anthony Fauci repeatedly denied ever funding gain-of-function research, let alone with respect to SARS-CoV-2. With this in mind, note one of the key sources of funding for this current research that has generated a super-deadly SARS-CoV-2; as disclosed by the authors…

“National Institutes of Health, NIAID grants R01 AI159945 (to SB and MS) and R37 AI087846 (to MUG)”

NIAID is the National Institute of Allergy and Infectious Diseases, of which Anthony Fauci is the director! I am keen to see if Fauci will still declare under oath that his agency has never funded gain-of-function research related to SARS-CoV-2.

Why The Chimeric SARS-CoV-2 Is More Dangerous Than Omicron

In most people, the Omicron variant of SARS-CoV-2 typically causes only mild COVID-19, if any disease at all. This is in large part due to it being limited to infecting only the upper airways. In contrast, earlier versions of SARS-CoV-2 could infect the lower airways in some people where it could cause severe pneumonia in high-risk individuals; a demographic that has been well-defined for most of the declared pandemic.

Some scientists have been forewarning that if a variant of SARS-CoV-2 were to emerge that had the infectivity and immunoevasive properties of Omicron, but could get deep into the lungs like earlier variants, the results could be deadly. With this in mind, here is what the authors of the pre-print article had to say about their virus…

“…unlike naturally occurring Omicron, [the chimeric SARS-CoV-2] efficiently replicates in cell lines and primary-like distal lung cells.”

…translation: the chimeric SARS-CoV-2 has the potential to cause infections deep in the lungs, where severe pneumonia would be the expected outcome.

We may have been on our way to naturally selecting such a variant of SARS-CoV-2 through the completely inappropriate global use of COVID-19 inoculations that apply a non-lethal selective pressure. Twenty-three American scientists have inadvertently provided the proof-of-principle that emergence of a potentially deadly SARS-CoV-2 is possible. The problem is, this virus is no longer theoretical. It potentially exists now; in laboratories in Boston.

It Gets Worse: Providing a Recipe for a Super-Pathogen

A good scientific paper should be written in such a way that other scientists in the respective field(s) of expertise could repeat the experiments to determine whether or not the results can be replicated. I am a viral immunologist and I reviewed the materials and methods section. I am confident that my research team could use this information to make the same chimeric virus. My team would never do this. However, I cannot speak to the morality of potential bioterrorists who could just as easily replicate the work should they have access to basic laboratory facilities.

In essence, the 23 authors of this paper have provided a recipe for a potentially potent bioterrorism agent. It is in the public domain and can no longer be eliminated from cyberspace.

Remarkably, It Gets Even Worse

The naturally occurring SARS-CoV-2 is what is known as a ‘containment level-3 (CL-3) pathogen’ (Americans would call it a ‘biological safety level-3 pathogen’). This means that research with this virus must be conducted in a CL-3 facility. Such facilities have sufficient biosecurity to keep a CL-3 pathogen contained. A major potential problem with gain-of-function research is that it can amplify the danger and/or infectivity of a pathogen. This is exactly what happened in the current case.

In short, the research project started with a non-lethal SARS-CoV-2. What emerged is a virus with the potential to be much more dangerous. This means that the 23 authors of the article may have ended up with a CL-4 pathogen housed in a CL-3 facility. The latter type of facility is not designed to contain a CL-4 pathogen.

This is an excerpt from the materials and methods section of the paper…

“All procedures were performed in a biosafety level 3 (BSL3) facility at the National Emerging Infectious Diseases Laboratories of the Boston University”

Here is how the United States Centers for Disease Control describe pathogens that must only be handled within CL-4 facilities…

“The microbes in a BSL-4 lab are dangerous and exotic, posing a high risk of aerosol-transmitted infections. Infections caused by these microbes are frequently fatal and without treatment or vaccines. Two examples of microbes worked with in a BSL-4 laboratory include Ebola and Marburg viruses.”

• Can SARS-CoV-2 be transmitted via aerosols? Yes

• Is the chimeric SARS-CoV-2 frequently fatal? Yes, in mice; unknown in humans

• Do effective treatments exist? The most effective ones have been outlawed

• Do effective vaccines exist? No. Laughable vaccine-wannabes exist, though.

So, should the chimeric SARS-CoV-2 have only been handled in a CL-4 facility. Likely yes, but, “All procedures were performed in a biosafety level 3 facility”.

If this virus were to get released into the public, it could result in a global catastrophe should its fatality rate, which is similar to ancestral SARS-CoV-2 be coupled with the much higher transmissibility of Omicron. Although this virus was not evaluated in humans, pre-clinical studies are used to try to predict what would happen in people. There is the theoretical potential for the virus to be less or equally deadly in people as compared to mice. However, for all we know, the virus could be even more deadly in people than it was in mice. The original SARS-CoV-2 did not prove to be particularly deadly in people, but it did not have anywhere near the transmission potential of the Omicron variant.

Action Must Be Taken Immediately: Reckless Science Must Be Stopped

1. Gain-of-function research with pathogens should be outlawed around the globe. Highly infectious viruses have no respect for borders.

2. Chimeric SARS-CoV-2, which has the potential to be a CL-4 pathogen, was handled under CL-3 conditions. All stocks of this virus should be destroyed as soon as possible. All people who worked with this virus and their contacts should be tested via sequencing to determine if there is any evidence of this synthetic virus having been released.

3. Agencies like Fauci’s NIAID should be investigated and questioned as to why they are actively funding gain-of-function research with SARS-CoV-2, which was itself the result of gain-of-function research. The fear-mongered over-reaction to the original version of their virus massively disrupted the global population. Continuing to manipulate this virus should be investigated as potential criminal behaviour.

4. The twenty three scientists who engineered a novel SARS-CoV-2 that could be much more dangerous than the original variant, as well as Boston University, should be investigated and their research sanctioned. They have demonstrated grossly reckless scientific behaviour.

5. Unfortunately, not much can be done about the fact that a recipe for potentially enhancing the danger of SARS-CoV-2 is now in the hands of any interested bioterrorists who have read or will read the pre-print article.

Gain-of-function research does not represent the only option to study pathogenicity and infectivity of a pathogen. Even if questions arise that cannot be definitively answered in the absence of gain-of-function research, those would be questions that should be left unanswered. Gain-of-function research can result in new versions of pathogens with difficult-to-predict behaviours. The risk exceeds any benefit. Science should not be practiced completely unfettered.

A Response to Queries About Alex Berenson’s Take on This Research

I have been asked about Alex Berenson’s very different take on the findings of this pre-print article. As such, I have added this section. You can find his article here. Generally, he downplays the potential dangers of the research outlined in this pre-print article. My take is that Alex has missed key points.

First, gain-of-function research can result in pathogens with unpredicted functions. Only a limited array of these functions were assessed in this study. Alex noted that mice are not humans. Of course, he is correct. But, he assumes that because the original variant of the virus was less fatal in people than mice that the chimeric one will be also. However, in the absence of data that assesses this, it is not a safe assumption to make. Assumptions have caused too many problems over the past 2.5 years. For all we know, the chimeric virus could be more dangerous in people than mice. We can’t know unless the appropriate study is conducted. I’m not going to volunteer for testing to determine how relatively dangerous or safe the chimeric virus is.

Alex went so far as to state "Nor did the researchers provide any evidence that the blended Omicron/wild-type coronavirus is able to defeat antibodies in people who have been infected with and recovered from Omicron". Much more importantly, the researchers did not provide evidence to assure anybody that antibodies in people can adequately protect against the new virus. In this instance, Alex seems to have lost sight of the precautionary principle. We should never assume the safety of a novel chimeric virus until it is definitively proven.

Alex missed another key point. Even if the original SARS-CoV-2 was a bit more lethal in mice than the chimeric version, it was also much less transmissible than Omicron. The danger of a virus to a population is not solely dependent on the severity of disease that it can cause. It also depends heavily on its potential to be transmitted throughout a population. A slightly less dangerous virus that is much more infectious would ultimately be more lethal within a population. Put another way, one would expect that a ‘souped-up’ (more lethal) version of the highly transmissible Omicron variant would be very dangerous. For example, Ebola and Marburg viruses have very high case fatality rates but don’t spread efficiently through populations (thank goodness). In contrast, influenza viruses have much lower case fatality rates but are much more infectious, thereby resulting in far higher numbers of cases. The result is that the annual flu kills more people than Ebola and Marburg viruses.

In short, Alex Berenson’s article makes too many assumptions, misses key aspects of the biology of pathogens, and fails to properly account for the precautionary principle. It gives me the impression that he might even find this type of gain-of-function research acceptable should there be some advanced disclosure that it is going to happen. He goes so far as to accuse those who are concerned about this as potentially contributing to the hysteria that has plagued our world for 2.5 years now. Raising legitimate concerns and calling for an end to potentially dangerous gain-of-function research is not fear-mongering. It is a call to place limits on reckless science that has the potential to cause catastrophic harm.

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