zlacker

> The virus entered humans with it's spike protein already fully adapted to the human ACE receptor protein.

That's not really true. It was adapted to ACE but not perfectly. As the B117 shows it could do better. Coronaviruses mutate slowly and random mutation in the spike protein is a lot more likely to make non-functional than to improve it. It's good enough, not perfect. Evolution likes good enough.

EDIT: but you do raise a good point with how much better than the known coronaviruses' spikes it is. Perhaps there is another intermediate host with ACE2 closer to humans? Sars-Cov-2 infects pretty well lots of animals - almost all the cats, minks, ...

>>yread+(OP)
At least in silico, SARS-CoV-2 binds better to human ACE2 than for any other mammal tested. The only other animals in their "very high" category were primates with ACE2 very similar to human:

https://www.pnas.org/content/117/36/22311

Evolution doesn't require anything beyond "good enough", but it's surprising for a virus to be better-adapted to humans than to its animal hosts at the moment of its zoonotic jump--before the jump, where could that pressure come from? I don't think this is determinative, but it points weakly in favor of lab origin (e.g., from culture in human cells or in mice genetically engineered to express human ACE2).