At minimum, an explanation of how the linked research (which shows that the cleavage sites are indeed common, as the parent comment explained) is somehow wrong. It doesn’t make any sense to insist they aren’t common in response to a paper showing specific examples of them occurring in nearby SARS-CoV-2 ancestors.
You badly broke the site guidelines repeatedly in this thread, and you also discredited your own case by giving open-minded readers a strong reason to discount what you're saying. None of that does anybody any good, so please stop doing it.
Obviously we moderate and eventually ban accounts that post like this—we have to, or this place will destroy itself even faster than it already is. But regardless of whether that moves you or not, you should take in the point that by being an asshole in the comments, you're creating the very situation that is presumably frustrating you in the first place, by discrediting the view that you believe to be the truth.
It would be far more in your interest to make your substantive points neutrally, thoughtfully, and respectfully. Then you wouldn't be undermining your own argument so badly. See https://hn.algolia.com/?dateRange=all&page=0&prefix=true&sor... for past explanations.
The point was that the furin cleavage site does appear in other Coronaviruses, and therefore it’s not a random appearance in this one.
The specific details of the paper you’re nit-picking aren’t relevant. The sequence either appears elsewhere or it doesn’t, but it clearly appears elsewhere in Coronaviruses.
Therefore, comparing the appearance of the sequence in another Coronavirus to random chance is a flawed comparison.
The next question, to my mind, is "How common is that cleavage site in other viruses, especially other viruses endemic to the origin location of SARS-Cov-2?" With a follow-up of "How possible would it be for multi-virus splicing to generate that sequence from two otherwise-unrelated, possibly damaged sequences ending up head-to-tail in the DNA of a host cell?"
We know of other novel viruses that have resulted from sequences of multiple viruses being spliced together in a living host naturally. I don't know how we'd disambiguate that possibility from human synthesis.
I'm sorry, that is simply not the case, neither at the protein level nor at the DNA level. Furin cleavage sites have diversity.
The canonical minimal furin cleavage site sequence is RX(R/K)R, which had a highly variable amino acid and a choice between the two basic amino acids in another position. This variability is sampled across the coronavirus furin cleavage site sequences.
