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COMMENT: We highlight information presented in FTR #1129, for purposes of emphasizing the flimsy nature of the argument presented in a paper from Nature Medicine.
Many scientific and medical people dismissing the argument that the Covid-19 coronavirus may have been created in a laboratory may be acting out of the sincere desire to preclude a full-dress Cold War between the U.S. and China. The Trump administration has tirelessly flogged the “China did it and it came from a laboratory” meme. Many liberals who dismissed the obvious fact that President Kennedy was murdered by a cabal of powerful U.S. national security interests did so because of what Peter Dale Scott calls a “level one cover-up”–alleged Soviet and/or Castro Cuban manipulation of Lee Harvey Oswald, fabricated by the executioners themselves.
That notwithstanding, there is abundant evidence of a man-made origin of the virus. (We do NOT believe that the event was authored–deliberately or accidentally–by China. The Covid-19 outbreak occurred in the middle of a “Full-Court-Press” covert and overt regime-change operation against China by the U.S. and its allies, and we feel that those interests are the executive elements behind the pandemic.)
Two telling, thoughtful, substantive critiques of the Nature Medicine article shed light on the flimsy nature of its arguments.
It would not be unfair to characterize the article as “The Warren Report” of the Covid-19 pandemic.
Like the Bible, it is open to serious scientific refutation: ” . . . . To put it simply, the authors are saying that SARS-CoV‑2 was not deliberately engineered because if it were, it would have been designed differently. However, the London-based molecular geneticist Dr Michael Antoniou commented that this line of reasoning fails to take into account that there are a number of laboratory-based systems that can select for high affinity RBD variants that are able to take into account the complex environment of a living organism. This complex environment may impact the efficiency with which the SARS-CoV spike protein can find the ACE2 receptor and bind to it. An RBD selected via these more realistic real-world experimental systems would be just as ‘ideal’, or even more so, for human ACE2 binding than any RBD that a computer model could predict. And crucially, it would likely be different in amino acid sequence. So the fact that SARS-CoV‑2 doesn’t have the same RBD amino acid sequence as the one that the computer program predicted in no way rules out the possibility that it was genetically engineered. . . .”
Dr. Michael Antoniou notes that different genetic engineering processes than the one highlighted in the Nature Medicine paper can be used: ” . . . . There is another method by which an enhanced-infectivity virus can be engineered in the lab. A well-known alternative process that could have been used has the cumbersome name of “directed iterative evolutionary selection process”. In this case, it would involve using genetic engineering to generate a large number of randomly mutated versions of the SARS-CoV spike protein receptor binding domain (RBD), which would then be selected for strong binding to the ACE2 receptor and consequently high infectivity of human cells. . . .”
The notion that the Nature Medicine authors had not heard of the above process is not credible: ” . . . . Such a directed iterative evolutionary selection process is a frequently used method in laboratory research. So there is little or no possibility that the Nature Medicine article authors haven’t heard of it – not least, as it is considered so scientifically important that its inventors were awarded the Nobel Prize in Chemistry in 2018. . . .”
Of more than passing significance is another article that finds serious fault with the Nature Medicine paper. ” . . . . Professor Stuart Newman, professor of cell biology and anatomy at New York Medical College, says that a key argument used to deny that it could be a genetically engineered strain that escaped from a laboratory actually points to the exact opposite. In other words, it indicates that SARS-CoV‑2 could well be genetically engineered and that it could have escaped from a lab. . . . As Adam Lauring, an associate professor of microbiology, immunology and infectious diseases at the University of Michigan Medical School, has noted, Andersen’s paper argues that, ‘the SARS-CoV‑2 virus has some key differences in specific genes relative to previously identified coronaviruses – the ones a laboratory would be working with. This constellation of changes makes it unlikely that it is the result of a laboratory ‘escape’.‘But Professor Newman says that this is totally unconvincing because ‘The ‘key differences’ were in regions of the coronavirus spike protein that were the subject of genetic engineering experiments in labs around the world (mainly in the US and China) for two decades.’ . . .”
Professor Newman goes on to highlight other, serious flaws in the argument: ” . . . In an email interview with GMWatch, Newman, who is editor-in-chief of the journal Biological Theory and co-author (with Tina Stevens) of the book Biotech Juggernaut, amplified this speculation by noting, ‘The Nature Medicine paper points to variations in two sites of the spike protein of the new coronavirus that the authors claim must have arisen by natural selection in the wild. However, genetic engineering of one of these sites, the ACE2 receptor binding domain, has been proposed since 2005 in order to help generate vaccines against these viruses (see this paper). It is puzzling that the authors of the Nature Medicine commentary did not cite this paper, which appeared in the prominent journal Science.’ Moreover, Newman added, “The second site that Andersen et al. assert arose by natural means, a target of enzyme cleavage not usually found in this class of viruses, was in fact introduced by genetic engineering in a similar coronavirus in a paper they do cite. This was done to explore mechanisms of pathogenicity. . . . .”
Worth noting, again, is the British Medical Association’s warning discussed in FTR #1129: ” . . . .The BMA report warns that legitimate research into microbiological agents and genetically targeted therapeutic agents could be difficult to distinguish from research geared towards developing more effective weapons. . . .”
As the GMWatch authors conclude: ” . . . . Such ‘enhanced infectivity’ research is carried out on viruses all over the world (and not just in China) to investigate their behaviour and to develop vaccines and other therapies, as well as for ‘biodefence’ purposes. . . .”
1. “Was the COVID-19 virus genetically engineered?” by Claire Robinson; GMWatch; 04/22/2020.
Since the COVID-19 pandemic took off, speculation has been rife about its origins. The truth is that nobody knows for certain how the virus first took hold. But despite that uncertainty, suggestions that the virus may have been genetically engineered, or otherwise lab-generated, have been rejected as “conspiracy theories” incompatible with the evidence.
Yet the main evidence that is cited as ending all speculation about the role of genetic engineering and as proving the virus could only have been the product of natural evolution turns out to be surprisingly weak. Let’s take a look at it.
The authors of a recently published paper in the journal Nature Medicine argue that the SARS-CoV‑2 virus driving the pandemic arose through natural mutation and selection in animal (notably bats and pangolins) or human hosts, and not through laboratory manipulation and accidental release. And they say they have identified two key characteristics of the virus that prove this: the absence of a previously used virus backbone and the way in which the virus binds to human cells.
Not the “ideal” design for infectivity?
As you would expect of a virus that can cause a global pandemic, SARS-CoV‑2 is good at infecting human cells. It does this by binding with high affinity (that is, it binds strongly) to the cell surface membrane protein known as angiotensin-converting enzyme 2 (ACE2), which enables it to enter human cells. But, basing their argument on a computer modelling system, the authors of the Nature Medicine paper argue that the interaction between the virus and the ACE2 receptor is “not ideal”.
They say that the receptor-binding domain (RBD) amino acid sequence of the SARS-CoV‑2 spike protein – the part of the spike protein that allows the virus to bind to the ACE2 protein on human cell surfaces – is different from those shown in the SARS-CoV family of viruses to be optimal for receptor binding.
They appear to argue, based on their and others‘ computer modelling data, that they have identified the “ideal” CoV spike protein RBD amino acid sequence for ACE2 receptor binding. They then seem to imply that if you were to genetically engineer SARS-CoV for optimal human ACE2 binding and infectivity, you would use the RBD amino acid sequence predicted by their computer modelling. But they point out that SARS-CoV‑2 does not have exactly the same computer program-predicted RBD amino acid sequence. Thus they conclude that it could not have been genetically engineered, stating: “This is strong evidence that SARS-CoV‑2 is not the product of purposeful manipulation.”
To put it simply, the authors are saying that SARS-CoV‑2 was not deliberately engineered because if it were, it would have been designed differently.
However, the London-based molecular geneticist Dr Michael Antoniou commented that this line of reasoning fails to take into account that there are a number of laboratory-based systems that can select for high affinity RBD variants that are able to take into account the complex environment of a living organism. This complex environment may impact the efficiency with which the SARS-CoV spike protein can find the ACE2 receptor and bind to it. An RBD selected via these more realistic real-world experimental systems would be just as “ideal”, or even more so, for human ACE2 binding than any RBD that a computer model could predict. And crucially, it would likely be different in amino acid sequence. So the fact that SARS-CoV‑2 doesn’t have the same RBD amino acid sequence as the one that the computer program predicted in no way rules out the possibility that it was genetically engineered.
Limits to computer modelling
Dr Antoniou said that the authors’ reasoning is not conclusive because it is based largely on computer modelling, which, he says, is “not definitive but only predictive. It cannot tell us whether any given virus would be optimized for infectivity in a real world scenario, such as in the human body. That’s because the environment of the human body will influence how the virus interacts with the receptor. You can’t model that accurately with computer modelling as there are simply too many variables to factor into the equation.”
Dr Antoniou added, “People can put too much faith in computer programs, but they are only a beginning. You then have to prove whether the computer program’s prediction is correct or not by direct experimentation in a living organism. This has not been done in the case of this hypothesis, so it remains unproven.”
It is even possible that SARS-CoV‑2 was optimized using a living organism model, resulting in a virus that is better at infecting humans than any computer model could predict.
More than one way to engineer a virus
The authors of the Nature Medicine article seem to assume that the only way to genetically engineer a virus is to take an already known virus and then engineer it to have the new properties you want. On this premise, they looked for evidence of an already known virus that could have been used in the engineering of SARS-CoV‑2.
And they failed to find that evidence. They stated, “Genetic data irrefutably show that SARS-CoV‑2 is not derived from any previously used virus backbone.”
But Dr Antoniou told us that while the authors did indeed show that SARS-CoV‑2 was unlikely to have been built by deliberate genetic engineering from a previously used virus backbone, that’s not the only way of constructing a virus. There is another method by which an enhanced-infectivity virus can be engineered in the lab.
A well-known alternative
A well-known alternative process that could have been used has the cumbersome name of “directed iterative evolutionary selection process”. In this case, it would involve using genetic engineering to generate a large number of randomly mutated versions of the SARS-CoV spike protein receptor binding domain (RBD), which would then be selected for strong binding to the ACE2 receptor and consequently high infectivity of human cells.
This selection can be done either with purified proteins or, better still, with a mixture of whole coronavirus (CoV) preparations and human cells in tissue culture. Alternatively, the SARS-CoV spike protein variants can be genetically engineered within what is known as a “phage display library”. A phage is a virus that infects bacteria and can be genetically engineered to express on its exterior coat the CoV spike protein with a large number of variants of the RBD. This preparation of phage, displaying on its surface a “library” of CoV spike protein variants, is then added to human cells under laboratory culture conditions in order to select for those that bind to the ACE2 receptor.
This process is repeated under more and more stringent binding conditions until CoV spike protein variants with a high binding affinity are isolated.
Once any of the above selection procedures for high affinity interaction of SARS-CoV spike protein with ACE2 has been completed, then whole infectious CoV with these properties can be manufactured.
Such a directed iterative evolutionary selection process is a frequently used method in laboratory research. So there is little or no possibility that the Nature Medicine article authors haven’t heard of it – not least, as it is considered so scientifically important that its inventors were awarded the Nobel Prize in Chemistry in 2018.
Yet the possibility that this is the way that SARS-CoV‑2 arose is not addressed by the Nature Medicine article authors and so its use has not been disproven.
No proof SARS-CoV‑2 was not genetically engineered
In sum, the Nature Medicine article authors offer no evidence that the SARS-CoV‑2 virus could not have been genetically engineered. That’s not to say that it was, of course. We can’t know one way or the other on the basis of currently available information.
Dr Antoniou wrote a short letter to Nature Medicine to point out these omissions in the authors’ case. Nature Medicine has no method of submitting a simple letter to the editor, so Dr Antoniou had to submit it as a Matters Arising commentary, which the journal defines as presenting “challenges or clarifications” to an original published work.
Dr Antoniou’s comments were titled, “SARS-CoV‑2 could have been created through laboratory manipulation”. However, Nature Medicine refused to publish them on the grounds that “we do not feel that they advance or clarify understanding” of the original article. The journal offered no scientific argument to rebut his points.
In our view, those points do offer clarification to the original article, and what’s more, there is a strong public interest case for making them public. That’s why we reproduce Dr Antoniou’s letter below this article, with his permission.
Not genetic engineering – but human intervention
There is, incidentally, another possible way that SARS-CoV‑2 could have been developed in a laboratory, but in this case without using genetic engineering. This was pointed out by Nikolai Petrovsky, a researcher at the College of Medicine and Public Health at Flinders University in South Australia. Petrovsky says that coronaviruses can be cultured in lab dishes with cells that have the human ACE2 receptor. Over time, the virus will gain adaptations that let it efficiently bind to those receptors. Along the way, that virus would pick up random genetic mutations that pop up but don’t do anything noticeable.
“The result of these experiments is a virus that is highly virulent in humans but is sufficiently different that it no longer resembles the original bat virus,” Petrovsky said. “Because the mutations are acquired randomly by selection, there is no signature of a human gene jockey, but this is clearly a virus still created by human intervention.”
Dr Antoniou agrees that this method is possible – but he points out that waiting for nature to produce the desired mutations is a lot slower than using genetic engineering to generate a large number of random mutations that you can then select for the desired outcome by a directed iterative evolutionary procedure.
Because genetic engineering greatly speeds up the process, it is by far the most efficient way to generate novel pathogenic viruses in the lab. . . .
Conclusion
It is clear that there is no conclusive evidence either way at this point as to whether SARS-CoV‑2 arose by natural mutation and selection in animal and/or human hosts or was genetically engineered in a laboratory. And in this light, the question of where this virus came from should continue to be explored with an open mind.
*****
SARS-CoV‑2 could have been created through laboratory manipulation
Dr Michael Antoniou
Kristian Andersen and colleagues (“The proximal origin of SARS-CoV‑2”, Nature Medicine, 26: 450–452, 2020) argue that their amino acid sequence comparisons and computational modelling definitively proves that SARS-CoV‑2 has arisen through natural mutation and selection in animal or human hosts, and not through laboratory manipulation and accidental release. However, although the authors may indeed be correct in how they perceive SARS-CoV‑2 to have arisen, the data they present does not exclude the possibility that this new coronavirus variant could have been created through an in vitro, directed iterative evolutionary selection process (see https://en.wikipedia.org/wiki/Directed_evolution). Using this method, a very large library of randomly mutagenized coronavirus spike proteins could be selected for strong binding to the ACE2 receptor and consequently high infectivity of human cells. The power of such directed evolution to select for optimal enzymatic and protein-protein interactions was acknowledged by the award of the Nobel Prize in Chemistry in 2018 (see https://www.nobelprize.org/prizes/chemistry/2018/summary/).
Another expert on biotechnology has attacked the evidence being used to quash suggestions that SARS-CoV‑2, the virus strain that causes COVID-19, might have been genetically engineered. Professor Stuart Newman, professor of cell biology and anatomy at New York Medical College, says that a key argument used to deny that it could be a genetically engineered strain that escaped from a laboratory actually points to the exact opposite. In other words, it indicates that SARS-CoV‑2 could well be genetically engineered and that it could have escaped from a lab.
The evidence that is being cited as proving that SARS-CoV‑2 is “not a laboratory construct or a purposefully manipulated virus” is a paper published by the immunologist Kristian Andersen and colleagues in Nature Medicine. As Adam Lauring, an associate professor of microbiology, immunology and infectious diseases at the University of Michigan Medical School, has noted, Andersen’s paper argues that, “the SARS-CoV‑2 virus has some key differences in specific genes relative to previously identified coronaviruses – the ones a laboratory would be working with. This constellation of changes makes it unlikely that it is the result of a laboratory ‘escape’.”
But Professor Newman says that this is totally unconvincing because “The ‘key differences’ were in regions of the coronavirus spike protein that were the subject of genetic engineering experiments in labs around the world (mainly in the US and China) for two decades.”
So not only does Newman think that the virus could have escaped from a lab, he also thinks that it could have originated in a virus stock that had undergone genetic engineering at some point.
In an email interview with GMWatch, Newman, who is editor-in-chief of the journal Biological Theory and co-author (with Tina Stevens) of the book Biotech Juggernaut, amplified this speculation by noting, “The Nature Medicine paper points to variations in two sites of the spike protein of the new coronavirus that the authors claim must have arisen by natural selection in the wild. However, genetic engineering of one of these sites, the ACE2 receptor binding domain, has been proposed since 2005 in order to help generate vaccines against these viruses (see this paper). It is puzzling that the authors of the Nature Medicine commentary did not cite this paper, which appeared in the prominent journal Science.”
Moreover, Newman added, “The second site that Andersen et al. assert arose by natural means, a target of enzyme cleavage not usually found in this class of viruses, was in fact introduced by genetic engineering in a similar coronavirus in a paper they do cite. This was done to explore mechanisms of pathogenicity.”
Newman said that he does not believe that these changes were deliberately introduced to increase the pathogenicity of any single strain, but that SARS-CoV‑2 may have had genetically engineered components in its history before being inadvertently introduced into the human population.
Newman is not the only scientist that has spoken out about the possibility of a genetically engineered element to the virus. We recently published an article in which the molecular geneticist Dr Michael Antoniou also cast doubt on assertions that the virus was not genetically engineered. Dr Antoniou set out a method by which the virus could have been genetically manipulated and selected for increased infectivity in the laboratory.
Neither Dr Antoniou, nor Prof Newman, nor we ourselves make any suggestion that, in the event that genetic engineering was involved, the intention was to create a bioweapon. Such “enhanced infectivity” research is carried out on viruses all over the world (and not just in China) to investigate their behaviour and to develop vaccines and other therapies, as well as for “biodefence” purposes. . . .
Banking with Bin Laden
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