Missing from this plausible scenario, of course, is any mention of Dr.
Fauci's $3.7 million grant to that very lab, after funding of such
"gain-of-function" research had been banned:

https://www.dailymail.co.uk/news/article-8211257/Wuhan-lab-performing-experiments-bats-coronavirus-caves.html

MCM

> Blocked on facebook.
>
>
> https://www.zerohedge.com/medical/rogue-chinese-virologist-joins-twitter-publishes-evidence-covid-19-created-lab
> 'Rogue' Chinese Virologist Joins Twitter, Publishes "Smoking Gun" Evidence
> COVID-19 Created In Lab
> [image: Profile picture for user Tyler Durden]
> <https://www.zerohedge.com/users/tyler-durden>
> *by * *Tyler Durden <https://www.zerohedge.com/users/tyler-durden>*
> Mon, 09/14/2020 - 11:35
>
> On Saturday we reported that Dr. Li-Meng Yan
> <https://www.zerohedge.com/geopolitical/chinese-doctor-claims-she-has-evidence-coronavirus-was-created-lab?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+zerohedge%2Ffeed+%28zero+hedge+-+on+a+long+enough+timeline%2C+the+survival+rate+for+everyone+drops+to+zero%29>
> - 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*.
>
>
> <https://www.zerohedge.com/s3/files/inline-images/yan%201a.PNG?itok=NGmp6oYA>
>
> On Sunday, *Li-Meng joined Twitter
> <https://twitter.com/LiMengYAN119?s=21> - *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
>
> 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.
>
> 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.
>
>
> <https://www.zerohedge.com/s3/files/inline-images/yan%201.jpg?itok=vqc5uevP>
>
> Similar to what is observed for other viral proteins, S2 of SARS-CoV-2
> shares a high sequence identity (95%) with S2 of ZC45/ZXC21. In stark
> contrast, between SARS-CoV-2 and ZC45/ZXC21, the S1 protein, which dictates
> which host (human or bat) the virus can infect, is much less conserved with
> the amino acid sequence identity being only 69%.
>
> Figure 4 shows the sequence alignment of the Spike proteins from six β
> coronaviruses. Two are viruses isolated from the current pandemic
> (Wuhan-Hu-1, 2019-nCoV_USA-AZ1); two are the suspected template viruses
> (Bat_CoV_ZC45, Bat_CoV_ZXC21); two are SARS coronaviruses (SARS_GZ02,
> SARS). The RBM is highlighted in between two orange lines. Clearly, despite
> the high sequence identity for the overall genomes, the RBM of SARS-CoV-2
> differs significantly from those of ZC45 and ZXC21. *Intriguingly, the
> RBM of SARS-CoV-2 resembles, on a great deal, the RBM of SARS Spike.
> Although this is not an exact “copy and paste”, careful examination of the
> Spike-hACE2 structures37,38 reveals that all residues essential for either
> hACE2 binding or protein folding (orange sticks in Figure 3C and what is
> highlighted by red short lines in Figure 4) are “kept”. *
>
> Most of these essential residues are precisely preserved, including those
> involved in disulfide bond formation (C467, C474) and electrostatic
> interactions (R444, E452, R453, D454), which are pivotal for the structural
> integrity of the RBM (Figure 3C and 4). The few changes within the group of
> essential residues are almost exclusively hydrophobic “substitutions”
> (I428àL, L443àF, F460àY, L472àF, Y484àQ), which should not affect either
> protein folding or the hACE2-interaction. At the same time, majority of the
> amino acid residues that are non-essential have “mutated” (Figure 4, RBM
> residues not labeled with short red lines). *Judging from this sequence
> analysis alone, we were convinced early on that not only would the
> SARS-CoV-2 Spike protein bind hACE2 but also the binding would resemble,
> precisely, that between the original SARS Spike protein and hACE223. Recent
> structural work has confirmed our prediction.*
>
>
> <https://www.zerohedge.com/s3/files/inline-images/yan%20fig%202.jpg?itok=riAtYLYh>
>
> 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."*
>
> It gets better, because the Chinese scientists then presciently tried to
> cover their tracks:
>
> Although it may be convenient to copy the exact sequence of SARS RBM, it
> would be too clear a sign of artificial design and manipulation. *The
> more deceiving approach would be to change a few nonessential residues,
> while preserving the ones critical for binding. *This design could be
> well-guided by the high-resolution structures (Figure 3)37,38. This way,
> when the overall sequence of the RBM would appear to be more distinct from
> that of the SARS RBM, the hACE2-binding ability would be well-preserved. We
> believe that *all of the crucial residues (residues labeled with red
> sticks in Figure 4, which are the same residues shown in sticks in Figure
> 3C) should have been “kept”. *As described earlier, while some should be
> direct preservation, some should have been switched to residues with
> similar properties, *which would not disrupt hACE2-binding and may even
> strengthen the association further [ZH: i.e., the virus was weaponized and
> enchanced]. *Importantly, changes might have been made intentionally at
> non-essential sites, making it less like a “copy and paste” of the SARS RBM.
>
> Yan also discusses the infamous furin-cleavage site:
>
> ... a close examination of the nucleotide sequence of the furin-cleavage
> site in SARS-CoV-2 spike has revealed that the two consecutive Arg residues
> within the inserted sequence (- PRRA-) are both coded by the rare codon CGG
> (least used codon for Arg in SARS-CoV-2) (Figure 7).
>
> <https://www.zerohedge.com/s3/files/inline-images/FAUL.jpg?itok=7gTS5l2n>
>
> In fact, this CGGCGG arrangement is the only instance found in the
> SARS-CoV-2 genome where this rare codon is used in tandem. *This
> observation strongly suggests that this furin-cleavage site should be a
> result of genetic engineering*. Adding to the suspicion, a FauI
> restriction site is formulated by the codon choices here, suggesting the
> possibility that the restriction fragment length polymorphism, a technique
> that a WIV lab is proficient at, could have been involved. There, the
> fragmentation pattern resulted from FauI digestion could be used to monitor
> the preservation of the furin-cleavage site in Spike as this furin-cleavage
> site is prone to deletions in vitro. Specifically, RT-PCR on the spike gene
> of the recovered viruses from cell cultures or laboratory animals could be
> carried out, the product of which would be subjected to FauI digestion.
> Viruses retaining or losing the furin-cleavage site would then yield
> distinct patterns, allowing convenient tracking of the virus(es) of
> interest.
>
> And another critical allegation: once again, the Wuhan Researchers were
> doing everything in their power to weaponize and boost the "*enhancement
> of the infectivity and pathogenicity of the laboratory-made coronavirus":*
>
> The evidence collectively suggests that the furin-cleavage site in the
> SARS-CoV-2 Spike protein may not have come from nature and could be the
> result of genetic manipulation. The purpose of this manipulation could have
> been to assess any potential *enhancement of the infectivity and
> pathogenicity of the laboratory-made coronavirus*.
>
> Summarizing the above:Evidence presented in this part reveals that certain
> aspects of the SARS-CoV-2 genome are extremely difficult to reconcile to
> being a result of natural evolution. The alternative theory we suggest is
> that the virus may have been created by using ZC45/ZXC21 bat
> coronavirus(es) as the backbone and/or template. *The Spike protein,
> especially the RBM within it, should have been artificially manipulated,
> upon which the virus has acquired the ability to bind hACE2 and infect
> humans. *This is supported by the finding of a unique restriction enzyme
> digestion site at either end of the RBM. An unusual furin-cleavage site may
> have been introduced and inserted at the S1/S2 junction of the Spike
> protein, *which contributes to the increased virulence and pathogenicity
> of the virus. *
>
> These transformations have then staged the SARS CoV-2 virus to eventually
> become a highly-transmissible, onset-hidden, lethal, sequelae-unclear, and
> massively disruptive pathogen.
>
> *Evidently, the possibility that SARS-CoV-2 could have been created
> through gain-of-function manipulations at the WIV is significant and should
> be investigated thoroughly and independently.*
>
> Finally, those curious how the virus could have been created synthetically
> in Wuhan, here is a diagram proposed by Dr. Yan explaining all the required
> steps:
>
>
> <https://www.zerohedge.com/s3/files/inline-images/how%20virus%20was%20created.jpg?itok=05RS3USB>
>
> Her full paper is below:
>
> And for those who missed it, here's Li-Meng's interview on UK television:
>
> As a reminder, Zero Hedge was banned from Twitter on Jan 31 for making
> just this allegation, following a hit-piece written by an alleged
> pedophile
> <https://www.zerohedge.com/political/buzzfeed-journo-reportedly-blogged-about-pedo-fantasies-rape-jokes-and-doxing>
> (who was later fired for plagiarism
> <https://www.zerohedge.com/political/buzzfeed-reporter-who-got-zerohedge-banned-twitter-fired-plagiarism>)
> and countless so-called "scientists" screaming that our take was fake news
> and nothing but propaganda. Five months later Twitter admitted it had
> made a mistake
> <https://www.zerohedge.com/markets/twitter-reinstates-zerohedge-after-admitting-it-made-error>,
> stating "we made an error in our enforcement action in this case."
>
>
>
---

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