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Unfortunately of Alina this and entire fabrication of the current state of knowledge
https://twitter.com/WashburneAlex/status/1761435036774027610This 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
https://twitter.com/stuartjdneil/status/1649033068257091584?s=202. 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.
https://twitter.com/SystemsVirology/status/16470257813890252802. 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.
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.