>You're comparing apples and oranges. 14 mutational sites across a virus with 17k ssDNA genome is not comparable to RATG-13 vs SARS-2, which have not just 1200 mutations different, they're spread out over HUNDREDS of SNPs.
If memory serves, that was a single generation. An rdrp produces one error per thousand bases, which comes out to 30 mutations per generation, so we're talking 40 generations away? That hardly seems significant.
>Not particularly. CGG exists in MERS 15 times. NL63, 29 times. It even exists twice in a row in Human coronavirus 229E. Throughout all of the known alphacoronaviruses (94 described) CGG exists 1575 times. In betacoronaviruses, it exists more times than my processor can count without hanging, and I believe it tops out at 9,999 events.
How many of those are in frame for an amino acid? How many of those are two in frame for arginine in a protein, next to each other?
>Why is it so unlikely that synonymous mutational drift over the course of 70 years of infections in millions of viral generations could create these arginine codons that are not the most optimized but still work in the mammals this virus infects? CGG works. It makes an arginine when this virus infects its host.
There are many reasons why it's unlikely. The first is pure statistics. But the statistics are almost certainly influenced by millions of years of biology.
>Why couldn't it be a recombination event between SARS-2 and one of the known coronaviruses with an extremely similar cleavage site?
It's absolutely possible and I would never dispute this. The possibility of it isn't a refutation of the possibility of other hypotheses, and I don't think it's in the scientific spirit to discount other viable hypotheses.