This really can't be taken seriously if they don't even bother addressing the BANAL-52 or RmYN02 sequences which very nearly have a functioning FCS: https://ib

This really can't be taken seriously if they don't even bother addressing the BANAL-52 or RmYN02 sequences which very nearly have a functioning FCS: https://ibb.co/T1YtShy https://ibb.co/T1YtShy There is a QTQTN deletion in circulating SARS-CoV-2 at the flanking region at 675-679 which has been observed in circulating human strains at the level of a few percent along with mouse-adapted strains. RmYN02 is closer in nucleotide sequences to those variants of SARS-CoV-2 than to ancestral (the SARS-CoV-2 variants carrying that deletion not show in that figure). If there are variants of RmYNO2 which retain the QTQT sequence at 675-679 then that virus would be one amino acid insertion away from a functioning QTQTNSPRAAR FCS sequence. Then flipping another amino acid would give the SARS-CoV-2 sequence. The relative probably would be discovered with a higher level of surveillance and sequencing of sarbecoviruses in wildlife. And the rest of the argument in this paper is some weird genetic numerology.