Dr. Steven Quay, who holds both a master’s and a doctorate degree from the University of Michigan, and Richard Muller, emeritus professor of physics at the University of California–Berkeley, said that two key pieces of evidence—one relating to gene splicing and the other to a lack of virus diversity—strongly suggest a lab origin regarding the outbreak that has infected more than 173 million people worldwide.
“The presence of the double CGG sequence is strong evidence of gene splicing, and the absence of diversity in the public outbreak suggests gain-of-function acceleration. The scientific evidence points to the conclusion that the virus was developed in a laboratory,” the pair wrote.
Gain-of-function research involves manipulating a virus’s genome to increase its virulence or transmissibility to better understand and predict the emergence of disease-causing agents and make it easier to come up with a solution before the disease emerges as a pandemic. Quay and Muller wrote that the most common genome pairing used in gain-of-function experiments on coronaviruses is CGG-CGG, or double CGG, which is spliced into a “prime location” in the genome, spurring the production of two arginine amino acids in a row and boosting a virus’s lethality.
This “alters the virus spike protein, rendering it easier for the virus to inject genetic material into the victim cell. Since 1992 there have been at least 11 separate experiments adding a special sequence to the same location. The end result has always been supercharged viruses,” the scientists wrote.
Genomic insertion can take place naturally in a process called recombination, but in cases of natural splicing, one of 35 other possible genomic sequences would be far more likely to appear than the double CGG, Quay and Muller wrote.
“In the entire class of coronaviruses that includes CoV-2, the CGG-CGG combination has never been found naturally,” they wrote. “That means the common method of viruses picking up new skills, called recombination, cannot operate here. A virus simply cannot pick up a sequence from another virus if that sequence isn’t present in any other virus.”
But in lab-based gain-of-function experiments, the CGG sequence is the pair of choice, they said.
“That’s because it is readily available and convenient, and scientists have a great deal of experience inserting it,” the scientists wrote. “An additional advantage of the double CGG sequence compared with the other 35 possible choices: It creates a useful beacon that permits the scientists to track the insertion in the laboratory.”
While the pair acknowledged that the double CGG sequence could have appeared naturally in SARS-CoV-2, the scientific term for the CCP virus, the fact that it’s present in the virus puts the burden of proof on opponents of the lab theory.
“Proponents of zoonotic origin must explain why the novel coronavirus, when it mutated or recombined, happened to pick its least favorite combination, the double CGG. Why did it replicate the choice the lab’s gain-of-function researchers would have made?” they wrote.
“At the minimum, this fact—that the coronavirus, with all its random possibilities, took the rare and unnatural combination used by human researchers—implies that the leading theory for the origin of the coronavirus must be laboratory escape.”
While the thesis that the virus leaked from a lab at the Wuhan Institute of Virology was initially dismissed by a number of prominent scientists, including White House adviser Dr. Anthony Fauci, there’s recently been a pivot. Fauci has acknowledged that he’s no longer certain the virus didn’t leak from the lab, while President Joe Biden has ordered U.S. intelligence to “redouble” its efforts to examine both theories, which he characterized as equally plausible.
Quay and Muller said the second key piece of evidence that supports a lab leak theory has to do with the genetic diversity of the CCP virus compared to the coronaviruses that caused SARS and MERS.
SARS and MERS, which were confirmed to be of natural origin, “evolved rapidly as they spread through the human population, until the most contagious forms dominated.”
Yet the CCP virus “appeared in humans already adapted into an extremely contagious version,” the pair noted, with no significant mutations occurring in the virus until months after the outbreak.
“Such early optimization is unprecedented, and it suggests a long period of adaptation that predated its public spread,” they wrote, arguing that there’s only one way this could be achieved, namely through “simulated natural evolution” by growing the virus on human cells under lab conditions.
