Postdoctoral researcher at the Broad Institute of MIT and Harvard 
Co-author of VIRAL: the search for the origin of Covid-19 
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My position on this: I don't know. Someone should be looking into the origins of RaTG13 and GD pangolin CoV. What was the sampling+sequencing process? Are there still ways to verify these samples (the former has disintegrated)? Were similar viruses discovered but not reported?
What I do know: claiming SARS2 was derived from the Zhoushan viruses that are >3000 mutations different -- this has destroyed the report's credibility, and, more importantly, diverted attention away from RaTG13, miners, and the missing WIV virus database (the 2nd Zenodo article).
Ok, on to (2). This 2nd claim relies on the 1st claim being true, which is, again, its greatest weakness. Instead of just going with "RBD was copied from another virus", Yan et al. perform enzymatic gymnastics to figure out how it could have gotten into the Zhoushan virus.
What claim (2) kind of gets correct - and I'm paraphrasing here - is that labs (including the WIV) have been codon optimizing spikes and swapping in RBMs to study receptor binding for over a decade. (Actually, this study did introduce an EcoRI site...) https://jvi.asm.org/content/82/4/1899 …
But this fixation on cloning sites is irrelevant to determining whether SARS2 was ever manipulated in a lab. Ralph Baric, UNC, long time collaborator of Shi, WIV says as much in his recent interview. *PLEASE RELEASE THE UNDUBBED VERSION*https://www.huffingtonpost.it/entry/e-possibile-creare-un-virus-in-laboratorio-senza-lasciare-traccia-la-risposta-dellesperto_it_5f5f3993c5b62874bc1f7339 …
Scientists have been able to clone coronavirus genomes seamlessly for years. They introduce cloning sites to show you that a genome has been manipulated. Another reason to retain a cloning site could be to monitor a feature, e.g. FCS, that tends to be lost during cell passage.
Which leads us to (3) the FCS - the most highly debated feature of SARS2. Why? SARS2 is the only SARS family virus (out of dozens, maybe 100s, sampled) with an S1/S2 FCS. The FCS has been actively researched, even in SARS1 & MERS, found to enhance virus tropism and infectivity.
Again, the fixation on whether there is a cloning site surrounding the FCS is unhelpful. The underlying thought here is that a lab could have been interested enough to follow up on earlier studies of introducing an FCS into SARS virus to see how it enhances pathogenicity.
For more details, please see this earlier thread - it is long and technical:https://twitter.com/Ayjchan/status/1266805310313967617 …
The rest of the Yan report delineates a cloning plan for creating the SARS2 genome, which, unfortunately, obscures critical observations with the terrible, terrible restriction cloning strategy and the desperation of somehow deriving SARS2 from the Zhoushan viruses.
The top points: 1. There are likely unpublished virus genomes closely related to SARS2. 2. The spike is generally modified alone before cloning into the larger genomic backbone. 3. Cloning can occur seamlessly. No need for RE site insertions! 4. It can be done in weeks-months.
5. There is a possibility of serial passaging in humanized mice or small animals. The WIV Science Magazine interview says these small animal experiments were conducted at BSL3 using SARS-like viruses.https://www.sciencemag.org/news/2020/07/trump-owes-us-apology-chinese-scientist-center-covid-19-origin-theories-speaks-out …
The Yan report ends by emphasizing the dangers of SARS2 and the importance of an independent audit of the WIV - which Peter Daszak, long time friend, collaborator, and funder of the Shi lab has now taken upon himself to lead the charge on.https://www.telegraph.co.uk/global-health/science-and-disease/scientists-examine-possibility-covid-leaked-lab-part-investigation/ …
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