On Saturday we reported that Dr. Li-Meng Yan – a Chinese virologist (MD, PhD) who fled the country, leaving her job at a prestigious Hong Kong university – appeared last week on British television where she claimed SARS-CoV-2, the virus which causes COVID-19, was created by Chinese scientists in a lab.
On Sunday, Li-Meng joined Twitter – and on Monday, just hours ago, she tweeted a link to a paper she co-authored with three other Chinese scientists titled:
Unusual Features of the SARS-CoV-2 Genome Suggesting Sophisticated Laboratory Modification Rather Than Natural Evolution and Delineation of Its Probable Synthetic Route
https://t.co/g9uPdcRIew— Dr. Li-Meng YAN (@LiMengYAN119) September 14, 2020
She also posted a link to her credentials on ResearchGate, revealing her (prior?) affiliation with The University of Hong Kong and 13 publications which have been cited 557 times.
https://t.co/u6SbFcR3IS— Dr. Li-Meng YAN (@LiMengYAN119) September 14, 2020
Cutting to the chase:
“The evidence shows that SARS-CoV-2 should be a laboratory product created by using bat coronaviruses ZC45 and/or ZXC21 as a template and/or backbone. Building upon the evidence, we further postulate a synthetic route for SARS-CoV-2, demonstrating that the laboratory-creation of this coronavirus is convenient and can be accomplished in approximately six months.
Here is the extended punchline:
The receptor-binding motif of SARS-CoV-2 Spike cannot be born from nature and should have been created through genetic engineering.
The Spike proteins decorate the exterior of the coronavirus particles. They play an important role in infection as they mediate the interaction with host cell receptors and thereby help determine the host range and tissue tropism of the virus. The Spike protein is split into two halves (Figure 3). The front or N-terminal half is named S1, which is fully responsible for binding the host receptor. In both SARS-CoV and SARS-CoV-2 infections, the host cell receptor is hACE2. Within S1, a segment of around 70 amino acids makes direct contacts with hACE2 and is correspondingly named the receptor-binding motif (RBM) (Figure 3C). In SARS-CoV and SARS-CoV-2, the RBM fully determines the interaction with hACE2. The C-terminal half of the Spike protein is named S2. The main function of S2 includes maintaining trimer formation and, upon successive protease cleavages at the S1/S2 junction and a downstream S2’ position, mediating membrane fusion to enable cellular entry of the virus.
By Tyler Durden
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