“Brief Summary of Evidence of Lab-Made 2019-nCoV” by Dr. Li-Meng Yan

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  • Tue, Aug 18, 2020 - 12:26pm

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    peakabu

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    “Brief Summary of Evidence of Lab-Made 2019-nCoV” by Dr. Li-Meng Yan

This paper was later revealed to be anonymously posted by Chinese whistleblower, Dr. Li-Meng Yan on 1/25/2020. In her paper, she presented evidence proving that the PLA-owned Zhoushan bat virus was the closest relative to 2019-nCoV before the RaTG13 sequence was suddenly published to the whole world out of nowhere on Jan 27.

Proofs:

Brief Summary of Evidence of Lab-Made 2019 nCoV

The first paper on 2019-nCoV published on Jan 21 authored by the Beijing Institute of Pharmacology and Toxicology (PLA-owned) and Chinese Academy of Sciences, as mentioned in her paper:

“Evolution of the novel coronavirus from the ongoing Wuhan outbreak and modeling of its spike protein for risk of human transmission”

  • Tue, Sep 15, 2020 - 02:00pm

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    Carsoner

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    “Brief Summary of Evidence of Lab-Made 2019-nCoV” by Dr. Li-Meng Yan

Their new paper was released:

 

Unusual Features of the SARS-CoV-2 Genome Suggesting Sophisticated Laboratory Modification Rather Than Natural Evolution and Delineation of Its Probable Synthetic Route

 

https://www.researchgate.net/publication/344240007_Unusual_Features_of_the_SARS-CoV-2_Genome_Suggesting_Sophisticated_Laboratory_Modification_Rather_Than_Natural_Evolution_and_Delineation_of_Its_Probable_Synthetic_Route

 

  • Thu, Sep 17, 2020 - 01:23pm

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    tbp

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    Li-Meng Yan paper summary

Unusual Features of the SARS-CoV-2 Genome Suggesting Sophisticated Laboratory Modification Rather Than Natural Evolution and Delineation of Its Probable Synthetic Route
September 14, 2020, by Yan, Li-Meng; Kang, Shu; Guan, Jie; Hu, Shanchang

Abstract:
The COVID-19 pandemic caused by the novel coronavirus SARS-CoV-2 has led to over 910,000 deaths worldwide and unprecedented decimation of the global economy. Despite its tremendous impact, the origin of SARS-CoV-2 has remained mysterious and controversial. The natural origin theory, although widely accepted, lacks substantial support. The alternative theory that the virus may have come from a research laboratory is, however, strictly censored on peer-reviewed scientific journals. Nonetheless, SARS-CoV-2 shows biological characteristics that are inconsistent with a naturally occurring, zoonotic virus. In this report, we describe the genomic, structural, medical, and literature evidence, which, when considered together, strongly contradicts the natural origin theory. 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. Our work emphasizes the need for an independent investigation into the relevant research laboratories. It also argues for a critical look into certain recently published data, which, albeit problematic, was used to support and claim a natural origin of SARS-CoV-2. From a public health perspective, these actions are necessary as knowledge of the origin of SARS-CoV-2 and of how the virus entered the human population are of pivotal importance in the fundamental control of the COVID-19 pandemic as well as in preventing similar, future pandemics.

Zero Hedge has an excellent summary:

As elaborated below, the way that SARS-CoV-2 RBM resembles SARS-CoV RBM and the overall sequence conservation pattern between SARS-CoV-2 and ZC45/ZXC21 are highly unusual. Collectively, this suggests that portions of the SARS-CoV-2 genome have not been derived from natural quasi-species viral particle evolution.

The paper then makes two critical observations for those who claim that SARS-CoV-2 has a natural origin: its RBM could have only been acquired in one of the two possible routes: 1) an ancient recombination event followed by convergent evolution or 2) a natural recombination event that occurred fairly recently.

She first dismisses option 1:

“this convergent evolution process would also result in the accumulation of a large amount of mutations in other parts of the genome, rendering the overall sequence identity relatively low. The high sequence identity between SARS-CoV-2 and ZC45/ZXC21 on various proteins (94-100% identity) do not support this scenario and, therefore, clearly indicates that SARS-CoV- 2 carrying such an RBM cannot come from a ZC45/ZXC21-like bat coronavirus through this convergent evolutionary route.”

She then dismisses option 2:

In the second scenario, the ZC45/ZXC21-like coronavirus would have to have recently recombined and swapped its RBM with another coronavirus that had successfully adapted to bind an animal ACE2 highly homologous to hACE2. The likelihood of such an event depends, in part, on the general requirements of natural recombination: 1) that the two different viruses share significant sequence similarity; 2) that they must co-infect and be present in the same cell of the same animal; 3) that the recombinant virus would not be cleared by the host or make the host extinct; 4) that the recombinant virus eventually would have to become stable and transmissible within the host species.

In regard to this recent recombination scenario, the animal reservoir could not be bats because the ACE2 proteins in bats are not homologous enough to hACE2 and therefore the adaption would not be able to yield an RBM sequence as seen in SARS-CoV-2. This animal reservoir also could not be humans as the ZC45/ZXC21-like coronavirus would not be able to infect humans. In addition, there has been no evidence of any SARS-CoV-2 or SARS-CoV-2-like virus circulating in the human population prior to late 2019. Intriguingly, according to a recent bioinformatics study, SARS-CoV-2 was well-adapted for humans since the start of the outbreak.

Which leaves just one option:

Only one other possibility of natural evolution remains, which is that the ZC45/ZXC21-like virus and a coronavirus containing a SARS-like RBM could have recombined in an intermediate host where the ACE2 protein is homologous to hACE2. Several laboratories have reported that some of the Sunda pangolins smuggled into China from Malaysia carried coronaviruses, the receptor-binding domain (RBD) of which is almost identical to that of SARS-CoV-227-29,31. They then went on to suggest that pangolins are the likely intermediate host for SARS-CoV-227-29,31. However, recent independent reports have found significant flaws in this data40-42. Furthermore, contrary to these reports27-29,31, no coronaviruses have been detected in Sunda pangolin samples collected for over a decade in Malaysia and Sabah between 2009 and 201943. A recent study also showed that the RBD, which is shared between SARS-CoV-2 and the reported pangolin coronaviruses, binds to hACE2 ten times stronger than to the pangolin ACE22, further dismissing pangolins as the possible intermediate host. Finally, an in silico study, while echoing the notion that pangolins are not likely an intermediate host, also indicated that none of the animal ACE2 proteins examined in their study exhibited more favorable binding potential to the SARS-CoV-2 Spike protein than hACE2 did. This last study virtually exempted all animals from their suspected roles as an intermediate host, which is consistent with the observation that SARS-CoV-2 was well-adapted for humans from the start of the outbreak. This is significant because these findings collectively suggest that no intermediate host seems to exist for SARS-CoV-2, which at the very least diminishes the possibility of a recombinant event occurring in an intermediate host.

Fast-forwarding to the smoking gun:

Given that RBM fully dictates hACE2-binding and that the SARS RBM-hACE2 binding was fully characterized by high-resolution structures (Figure 3)37,38, this RBM-only swap would not be any riskier than the full Spike swap. In fact, the feasibility of this RBM-swap strategy has been proven. In 2008, Dr. Zhengli Shi’s group swapped a SARS RBM into the Spike proteins of several SARS-like bat coronaviruses after introducing a restriction site into a codon-optimized spike gene (Figure 5C). They then validated the binding of the resulted chimeric Spike proteins with hACE2. Furthermore, in a recent publication, the RBM of SARS-CoV-2 was swapped into the receptor-binding domain (RBD) of SARSCoV, resulting in a chimeric RBD fully functional in binding hACE2 (Figure 5C)39. Strikingly, in both cases, the manipulated RBM segments resemble almost exactly the RBM defined by the positions of the EcoRI and BstEII sites (Figure 5C). Although cloning details are lacking in both publications39,47, it is conceivable that the actual restriction sites may vary depending on the spike gene receiving the RBM insertion as well as the convenience in introducing unique restriction site(s) in regions of interest. It is noteworthy that the corresponding author of this recent publication, Dr. Fang Li, has been an active collaborator of Dr. Zhengli Shi since 201049-53. Dr. Li was the first person in the world to have structurally elucidated the binding between SARS-CoV RBD and hACE238 and has been the leading expert in the structural understanding of Spike-ACE2 interactions. The striking finding of EcoRI and BstEII restriction sites at either end of the SARS-CoV-2 RBM, respectively, and the fact that the same RBM region has been swapped both by Dr. Shi and by her long-term collaborator, respectively, using restriction enzyme digestion methods are unlikely a coincidence. Rather, it is the smoking gun proving that the RBM/Spike of SARS-CoV-2 is a product of genetic manipulation.”

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