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.

These questions are answered in the op paper

> do you understand that there is no one "the sequence"?

The linked paper is, literally, about a specific sequence. That’s the paper we’re discussing in this comment section.

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.