re: Did Wuhan lab shutdown in October? Cellphone data fuels conspiracy theories

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I doubt that. You can watch YouTube videos and order kits online to edit genomes.

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It is important to clarify, however, that not every false hypothesis is a conspiracy theory. For instance, some researchers pointed out the presence of HIV-like segments in the SARS-CoV-2 genome and claimed, based on an incomplete investigation, that it is evidence of intentional manipulation. The presence of HIV-like segments is an observation that is clearly explained by natural acquisition of those segments in a manner similar to that in related naturally occurring bat coronaviruses such as ZC45 and ZXC21, which contain similar segments.

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Given that the 96.2% sequence match of bat RaTG13 and human SARS-CoV-2 is not enough to rule out even a chimeric origin, Andersen et al. analyzed the mutations in the receptor-binding domain (RBD) of SARS-CoV-2 and compared features of its spike protein with that of bat RaTG13, pangolin coronavirus, human SARS-CoV, and two bat SARS-like coronaviruses. They highlighted two notable features in SARS-CoV-2, particularly the optimized binding of the spike protein of SARS CoV-2 to human ACE2 receptor and the existence of a functional polybasic site at the two subunits of the spike of nonobvious function that’s likely a result of natural mutations. Their analysis of the mutations showed that the so called RaTG13 couldn’t have been the backbone of SARS-CoV-2 had it been chimeric, with many unverified assumptions.

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First, Andersen et al. don’t conduct independent sequencing of bat RaTG13 samples which were sampled in 2013 but only sequenced and uploaded to GenBank in 2020. Therefore, Andersen’s analysis is just an extension of the published work of Zhou et al. from the Wuhan Institute of Virology, which is one alleged source of a possible leak of the virus. Second, they assume that published information from a lab where a source is suspected is complete, and they don’t verify that bat RaTG13 is, indeed, the closest relative of human SARS-CoV-2 encountered by or known to the two labs where the origin or source is suspected.

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I find it interesting you skipped over those three paragraphs originally while claiming you read the whole thing.

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Given that the 96.2% sequence match of bat RaTG13 and human SARS-CoV-2 is not enough to rule out even a chimeric origin, Andersen et al. analyzed the mutations in the receptor-binding domain (RBD) of SARS-CoV-2 and compared features of its spike protein with that of bat RaTG13, pangolin coronavirus, human SARS-CoV, and two bat SARS-like coronaviruses. They highlighted two notable features in SARS-CoV-2, particularly the optimized binding of the spike protein of SARS CoV-2 to human ACE2 receptor and the existence of a functional polybasic site at the two subunits of the spike of nonobvious function that’s likely a result of natural mutations. Their analysis of the mutations showed that the so called RaTG13 couldn’t have been the backbone of SARS-CoV-2 had it been chimeric, with many unverified assumptions.

However, after their brief and informative scientific endeavor, the authors then presented flawed arguments on the nature and source of the virus and conclusions that only reflect their beliefs and opinion. The approach they used to reach their conclusions is not sound for verification purposes, as it relies fundamentally on faith and trust. While trust is usual and healthy in academia, it’s not suitable for verification of lab accidents involving large-scale damage or potential WMD/dual use activity backed by a state.

First, Andersen et al. don’t conduct independent sequencing of bat RaTG13 samples which were sampled in 2013 but only sequenced and uploaded to GenBank in 2020. Therefore, Andersen’s analysis is just an extension of the published work of Zhou et al. from the Wuhan Institute of Virology, which is one alleged source of a possible leak of the virus. Second, they assume that published information from a lab where a source is suspected is complete, and they don’t verify that bat RaTG13 is, indeed, the closest relative of human SARS-CoV-2 encountered by or known to the two labs where the origin or source is suspected.

The conclusions of Andersen et al. on the nature of the virus almost all hinge on the assumption that they know all backbone viruses studied at the Wuhan lab, which reflects circular reasoning, given their sources and assumptions. The closest known virus to human SARS-CoV-2 and bat RaTG13 is bat BtCoV/4991—but only a partial sequence for the RdRp gene of BtCoV/4991 was uploaded to GenBank in 2016. It’s unclear if BtCoV/4991 is RaTG13 itself or a closer progenitor of SARS-CoV-2, because only a partial sequence was uploaded and BtCoV/4991 wasn’t referenced by Zhou et al. It’s unclear why it would be renamed.

Third, as professor Richard Ebright had pointed out, the authors dismiss the possibility that bat RaTG13 is a proximate progenitor of SARS-CoV-2 based on unverified assumptions on the evolutionary rates and about the possibility of passage in cell culture or animal models. While Andersen et al. do briefly acknowledge the possibility of passage in cell culture, they go on to assumptively conclude that the virus is natural in both origin and source when in fact a closely related bat coronavirus could have adapted to human cells in cell culture experiments.

Fourth, Andersen argued that discrepancies between the computational analysis work of one study they cited and experimental results is “strong evidence” of the absence of any purposeful manipulation of the virus. This argument should be dismissed as a reductionist fallacy, as it underestimates degrees of freedom and available types of computational analyses. Other scientists using molecular dynamics simulations showed that SARS-CoV-2 had a much higher binding affinity to human ACE2 receptors than SARS-CoV, with predictions in agreement with experiments.

The fact that Andersen’s discussion is flawed doesn’t say anything about the nature or the source of the virus. It, however, shows that their work can’t be considered conclusive and justifies further study on the origin and source of the virus.

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which took place held in Wuhan between October 18 and 27. As per Clouvel, doctors told her that it was likely that she had caught COVID-19. As per the recent reports, other French team members have also claimed that they also fell ill. But the French army has denied all knowledge of anyone contracting the disease during the games.

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Phylogenetic analysis of 30 publicly available SARS-CoV-2
samples concluded that emergence of SARS-CoV-2 in the
human population likely occurred in mid-November 2019.

LINK

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Estimates of the timing of the most recent common ancestor of SARS-CoV-2 made with current sequence data point to emergence of the virus in late November 2019

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Clinical data have shown that the date of
symptom onset of the first known patient
was 1 December 2019 [2]. Given the
known incubation period – between 1
and 14 days – the interspecies transmission could have occurred as late as
late November 2019.

LINK

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Given what’s known about the pace at which viral genomes mutate, if nCoV had been circulating in humans since significantly before the first case was reported on Dec. 8, the 24 genomes would differ more. Applying ballpark rates of viral evolution, Rambaut estimates that the Adam (or Eve) virus from which all others are descended first appeared no earlier than Oct. 30, 2019, and no later than Nov. 29.

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October would make sense, given that we started seeing cases in December.

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