The possibility that the outbreak may have started to evade the Wuhan Institute of Virology is attracting new attention. President Biden urged the national intelligence community to redouble its investigative efforts.
Much of the public discussion has focused on circumstantial evidence: mysterious diseases in late 2019; The lab deliberately worked by overloading viruses to increase the mortality rate (known as “getting a job” research). The Chinese Communist Party has been reluctant to release relevant information. Reports based on US intelligence indicated that the laboratory cooperated on projects with the Chinese military.
But the most compelling reason to favor the leak-in-lab hypothesis relies heavily on science. In particular, consider the genetic fingerprint of CoV-2, the new coronavirus responsible for Covid-19 disease.
In gain-of-function research, a microbiologist can dramatically increase the lethality of the coronavirus by attaching a special sequence in its genome at a key locus. This leaves no trace of tampering. But it alters the virus’ spike protein, making it easier for the virus to inject genetic material into the infected cell. Since 1992, there have been at least 11 separate experiments that have added private sequences to the same site. The end result has always been an overloaded virus.
The genome is the blueprint for the cell’s factory to produce proteins. The language consists of a three-letter “word”, with a total of 64 words, representing 20 different amino acids. For example, there are six different words for the amino acid arginine, which is the word often used in hypertrophic viruses. Each cell has a different preference for the word you most want to use.
If the work overload increases, other sequences can be cut at the same position. Instead of CGG-CGG (commonly known as “double CGG”) telling the protein factory to make two amino acids in a row from arginine, you’d get the same lethal force by connecting any of the other 35 two-word groups. arginine; If the insertion occurs naturally, eg by recombination, one of these 35 other sequences will likely appear; CGG is rarely used in the class of coronaviruses that can combine with CoV-2.
In fact, in the entire class of coronaviruses that includes CoV-2, the CGG-CGG complex is not found naturally. This means that the common method of viruses gaining new features, called recombination, cannot work here. A virus simply cannot take a sequence from another virus if that sequence is not present in any other virus.
Although double CGG is naturally avoided, the opposite is true in laboratory work. The chosen input sequence is the double CGG. This is because it is readily available and scientists have a lot of experience offering it. An added advantage of duplex CGG sequencing over 35 possible options: it creates a useful beacon that allows scientists to monitor placement in the lab.
Now the damned truth. This was the exact sequence seen in CoV-2. Animal proponents should explain why the new coronavirus, when mutated or recombined, chose the least preferred group, the CGG diploid group. Why repeat the choice that lab researchers might make for the job?
Yes, it could have happened by chance, by mutation. But do you believe it? At least, that fact — that the coronavirus, with all its random possibilities, has taken on a rare and abnormal mixture used by human researchers — means that the main theory about the coronavirus’ origin must be a lab leak.
When Shi Jingli and his lab colleagues published an article in February 2020 containing the partial genome of the virus, they omitted any mention of the special sequence that transmits the virus or the rare double section of CGG. However, the fingerprint can be easily identified in the data accompanying the card. Have you given up in the hope that no one will notice this evidence of the source of the company’s profits?
But within a few weeks, virologists Bruno Cotard and his colleagues had to published Sequence discovery in CoV-2 and its new supercharged site. There is a double CGG; You just have to look. In their article, they commented that the protein it stores “may provide the ability to gain function” for the virus, for “effective spread” to humans.
There is more scientific evidence pointing to the origin of CoV-2 gain of function. Even more compelling are the huge differences in the genetic diversity of CoV-2 compared to the coronaviruses responsible for SARS and MERS.
Both are of natural origin. Viruses evolved rapidly as they spread among humans until more infectious forms prevailed. Covid-19 didn’t work that way. It appeared in humans already adapted to a highly infectious version. No serious viral “improvement” occurred until a slight difference occurred several months later in England.
This rapid improvement is unprecedented and indicates a long period of adaptation that preceded its general spread. Science knows only one way to do this: mimicking natural evolution, growing the virus in human cells to an optimal level. This is exactly what you do when looking for a job. Mice genetically engineered to have the same coronavirus receptors as humans, called “humanized mice,” are often exposed to the virus to encourage adaptation.
The presence of the double CGG sequence is strong evidence for gene splicing, and the absence of diversity in the overall propulsion indicates an acceleration of gain-of-function. Scientific evidence leads to the conclusion that the virus was developed in a laboratory.
Dr. Kwai is the founder of Atossa Therapeutics and author of Stay Safe: A Doctor’s Guide to Surviving the Coronavirus. Mr. Mueller is Professor Emeritus of Physics at UC Berkeley and former chief scientist at Lawrence Berkeley National Laboratory.
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