> The virus entered humans with it's spike protein already fully adapted to the human ACE receptor protein.
1. Is a partially functional (still infectious) spike receptor protein possible? (you don't know, and present no evidence in this rant)
2. How do you know the virus shows "no accelerated evolution"...partially effective viruses would have a lower replication factor, and not become global pandemic, and would not spread far enough to preserved within the human population as anything of interest.
3. How do you know that a natural virus which was only partially effective at replication didn't in fact encounter favorable conditions when it encountered humans, having accidentally been better adapted for them?
> The fact that it doesn't mutate rapidly indicates it is near a strong local optimum.
4. How do you know that the spike protein - which is highly conserved amongst coronaviruses - can even have a range of mutations and still retain function (allowing viral entry to the cell for infectious purposes)? (you don't, research finds that the spike protein has suboptimal binding to ACE receptors - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7239051/)
> This stands in intense contrast to every other zoonotic transfer we know of.
5. Does it? Because no research is proposing this. Research in fact finds that analysis of similar coronaviruses shows that the spike protein is likely the result of multiple recombinations between a few species (https://academic.oup.com/emph/article/2020/1/290/5956769).
> Do we have evidence? What is the probability of this pattern occuring in the case of a natural spillover?
6. Do you? Apparently not because there's not a single shred of peer reviewed research you care to link to support your position here, and you've done none of the legwork to support the logic part of your conclusions.