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 w

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 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).