SARS CoV-2: a few features constantly misrepresented

1: a member of a family of viruses undergoing huge amounts of recombination in their natural host(s) as evidenced by family trees closest relatives in different parts of the genome. 2: Far from being ‘uniquely adapted to humans’ the RBDs of many of the family have broad specificity for mammalian ACE2s. The RBD of SARS2 exists in close relatives found in Laotian bats and pangolins. Not the product of ‘passage’

There is a very good reason Alex.

I have long been of the opinion that the new ELife publication system, while laudable in its intentions, leaves a door wide open to exploitation by motivated conspiracists like antivaxxers or those associated with their backers (brownstone/GBD).

https://twitter.com/WashburneAlex/status/1761435036774027610

This has always been my real objection to it, and given your activities over the last few years, and especially the egregiously motivated preprint that you constructed, that you would try your arm at ELife was a certainty IMO

1: For the NYT, Nature Op-eds et al. The key point of the HSM metagenomic data was that it PROVED that animal species that are reasonable suspects for an intermediary species were on sale at the time of the outbreak. 2. Despite the revisionism by the DRASTICs and those who sell books on the backs of their activities, this fact was both disputed by them (cf the ‘noone sells animals in November’ paper that has not been published), and most importantly DENIED by Chinese authorities to WHO..

1. Contrary to popular belief, most virologists I know are not cowboys when it comes to safety. They prefer to use far more tractable surrogate systems when studying dangerous viruses. A case study to highlight the nuances of viral manipulation, GoF etc.

https://twitter.com/stuartjdneil/status/1649033068257091584?s=20

2. Imagine you have related 2 bat viruses. One is a transmissible deadly human pathogen and must be studied at BSL4, the other is antigenically distinct but has caused no disease in the handful of people known to have been infected or in experimentally infected mice.

1. Something I haven’t seen much discussion of at #PathogensProject is about surrogate experimental systems for dangerous pathogens. 2. Predominantly from the retrovirus field, the establishment of lentiviral pseudotype systems (PLVs) for studying enveloped viral glycoproteins, as well as replication competent Rhabdovirus-based systems are cheap, easy and fast.

Opening statements (paraphrased)

Ratcliffe - Biden and those awful virologists are blocking the CIA agreeing with me
Feith - GoF is bad; and 3 sick WIV workers..
Lowenthal - intelliegence is diffcult and we may never get a straight answer.

So this is going to be revealing 🤦‍♂️ More paraphrasing

Feith - all scientists that dont agree about a lab leak are by definition conflicted.

1. The complexity of bat sarbecovirus-S/ Rhinolophus ACE2 interactions. Something you see stated all the time from LLers is that SARS2 is 'human-adapted'.

https://twitter.com/SystemsVirology/status/1647025781389025280

2. This notion, in part, is based on the SC2 spike receptor binding domain (RBD) binding and using the ACE2 of the ‘presumed’ bat reservoir (R affinis) much less efficiently than human ACE2 to enter cells.

1. Revisting this famous section from the DEFUSE grant proposal because I think we will be hearing a lot about it again. And let’s analyze what it actually says and compare it to the mantra of ‘they propsed to insert FCSs in bat CoVs” 2.Firstly thevirology because even 3 yrs, the authors of high profile books don’t get it (or don’t want to). For cell entry CoV spike proteins undergo at least 2 proteolytic cleavage steps by host cell protease enzymes. One is at the S1/S2 boundary, the other at the S2’ site.

1: The mark of any decent hypothesis is that it needs to account for all the existing evidence without exception. 2.That means accounting for the early cases (both the HSM-linked and unlinked cases) clustering with very high statistical significance with the market.