- Author: peacelv
- Editor: Jenny Ball
This article is published by Nicholas Wade, discussing the origin of COVID. The author said the virus that caused the pandemic is known officially as SARS-CoV-2, but can be called SARS2 for short. As many people know, there are two main theories about its origin. One is that it jumped naturally from wildlife to human. The other is that the virus was escaped from CCP’s lab. If we hope to prevent a second time such pandemic occurrence, it’s vital to find out the origin of the virus. The second theory is suggested by Dr. Li-Meng Yan.
The author described the two theories and explained why each was plausible, and then leave it for reader to see which one provided the better explanation with the available facts. The author said it’s important to note that so far there is no direct evidence for either theory. Each depends on a set of reasonable conjectures but so far lacks proof. So the author have only clues, not conclusions, to offer. But those clues point in a specific direction and the author is going to delineate some of the strands in this tangled skein of disaster.
The decoding of the virus’s genome showed it belonged a viral family known as beta-coronaviruses, to which the SARS1 and MERS viruses also belong. The relationship supported the idea that it was a natural virus that had managed to jump from bats as host to human. The wet market connection, the only other point of similarity with the SARS1 and MERS epidemics, was soon proved to be false: Chinese researchers found earlier cases in Wuhan with no link to the wet market.
Much of Dr. Shi’s work on gain-of-function in coronaviruses was performed at the BSL2 safety level, as is stated in her publications and other documents. She said in an interview with Science magazine that “The coronavirus research in our laboratory is conducted in BSL-2 or BSL-3 laboratories.”
The evidence above adds up to a serious case that the SARS2 virus could have been created in a lab, from which it then escaped. But the case, however substantial, falls short of proof. Proof would consist of evidence from the Wuhan Institute of Virology, or related labs in Wuhan, that SARS2 or a predecessor virus was under development there.
The CCP has made it unavailable of access to such records, another approach is to take certain salient facts about the SARS2 virus and ask how well each is explained by the two rival scenarios of origin, those of natural emergence and lab escape.
Here are four tests of the two hypotheses. Some technical details have been well analyzed in Dr. Li-Meng Yan’s first and second reports, but these are among the most persuasive for those who may care to follow the argument.
Dr. Yan said when you look for the fingerprints of a similar transition in SARS2, surprisingly the virus has hardly changed at all, at least until recently. From its very first appearance, it was well adapted to human cells. Researchers led by Alina Chan of the Broad Institute compared SARS2 with late stage SARS1, found that the two viruses were similarly well adapted, which by then was well adapted to human cells. “By the time SARS-CoV-2 was first detected in late 2019, it was already pre-adapted to human transmission to an extent similar to late epidemic SARS-CoV,” they wrote. And from the below four fields:
- The place of origin.
- Natural history and evolution
- The furin cleavage site
The furin cleavage site is a minute part of the virus’s anatomy but one that exerts great influence on its infectivity. It sits in the middle of the SARS2 spike protein. It also lies at the heart of the puzzle of where the virus came from. Because of all known SARS-related beta-coronaviruses, only SARS2 possesses a furin cleavage site. Which was well emphasized by Dr. Li-Meng Yan in her third report when she responded to the reviewers Warmbrod et al. All the other viruses have their S2 unit cleaved at a different site and by a different mechanism.
4) A Question of Codons
Here’s where it is interesting. Different organisms have different codon preferences. Human cells like to designate arginine with the codons CGT, CGC or CGG. But CGG is coronavirus’s least popular codon for arginine. Keep that in mind when looking at how the amino acids in the furin cleavage site are encoded in the SARS2 genome.
Only 5% of SARS2’s arginine codons are CGG, and the double codon CGG-CGG has not been found in any other beta-coronavirus. So how did SARS2 acquire a pair of arginine codons that are favored by human cells but not by coronaviruses?
From above, the author said it seemed more likely the virus is made in lab.
Dr. Li-Meng Yan demonstrated scientifically in her three reports.