I must say it, @K_G_Andersen never ends to surprise me with his compelling arguments... If you want to figure out why Wade is wrong you can Google it đŸ€ŁđŸ˜‚đŸ€Ł
Here he downplays the FCS of SARS2. These fragments do not really come and go all the time. I am not aware of experiments on CoV where the FCS arose by cell or animal passage. More on the FCS here:
https://twitter.com/Rossana38510044/status/1391282175392243717
Here he refers to RmYN02, which has no insertion at the S1/S2 cleavage site
https://arxiv.org/abs/2012.00627 
https://twitter.com/ydeigin/status/1373009214851932169
And to Gallaher's paper, with the fanciful theory of recombination on a train to Wuhan
Recombination is rare outside its group +
https://yurideigin.medium.com/btw-i-did-some-follow-up-reading-on-hku9-and-it-seems-it-cant-bind-ace2-or-dpp4-4370915065f6
As also my co-author @ydeigin says
https://twitter.com/ydeigin/status/1391499439773257729
the FCS could be not optimal because part of a vaccine attenuation strategy
https://twitter.com/Rossana38510044/status/1312414165768843267
Andersen admitted to be wrong with his prediction of the O-linked glycans
The FCS might be similar at the aa level to some FCoV sequences, but less at the nt level.
https://twitter.com/CZilcho/status/1388090961490743299
Andersen does not mention that the FCS binds extremely well to heparan sulphate as possible result of cell passage
https://link.springer.com/article/10.1007/s10311-021-01211-0
That the "P" is mutating towards residues creating more optimal furin sites could be reversion, which is not rare in live attenuated viruses, mostly if not completely attenuated because accidentally leaked.
"the exact (P)RRAR can be found in other coronaviruses." is true only at the amino acid level, not as nucleotides.
Andersen admits that the codon CGG is rare in CoV because it stimulates an immune reaction. It is only found in 3 % of arginine in SARS2. But he forgets to mention that CGG is double in the FCS, making it very special.
https://twitter.com/Rossana38510044/status/1312414075503206401
Nothing unusual here.
He forgets also to mention that by chance CGG is the best codon for arginine in humans, and CGA, used as second codon in FCoV is not that good (0.11 CGA vs 0.21 CGG)
https://www.genscript.com/tools/codon-frequency-table
And the fact that the FCS is remarkably stable and necessary for human-to-human transmission in a virus which had only few months to adapt to a new host might hint to previous cell passage in human airways cells, where it is stable or humanized mice.
So all the points from Andersen to disprove Baltimore’s observation on the FCS are false/misleading.
https://twitter.com/Merz/status/1391493018121760772
Actually our @Daoyu15 commented on this, but his replies have been hidden by @Merz. This is the way virologists welcome dissenting opinions.
https://twitter.com/Daoyu15/status/1391586915590152201 https://twitter.com/Daoyu15/status/1391589972621230080
Andersen does not take into account also the other special feature of SARS2, which is its special RBD adapted from the first isolate for very efficient human infection. He tried to justify it with its presence in the pangolin CoV MP789, which we can’t trust.
I recommend to listen to this old interview of Dr. Antoniou about the uncommon genetic features of SARS2
You can follow @Rossana38510044.
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