To answer below question, most bat CoV don't bind human ACE2 strongly, but can happen incidentally in evolution. Presumably because some mutations that increase binding to bat ACE2s incidentally increase binding to human ACE2, which has substantial homology to bat ACE2s. (1/6)
https://twitter.com/lab_leak/status/1446127423309770768
One example is recently described BANAL-20-52 bat CoV, which binds human ACE2 strongly (researchsquare.com/article/rs-871…). Another is SHC014 (ncbi.nlm.nih.gov/pmc/articles/P…), which @TheMenacheryLab @Baric_Lab showed infects human cells despite having evolved in bats. (2/6)
More broadly, we recently did large yeast-display survey of SARS-related CoV RBDs and found that some bind human ACE2 (and some ACE2s from other species) well despite being from bats (biorxiv.org/content/10.110…). (3/6) 
This promiscuous ACE2 binding must be quite common, because EcoHealth/WIV R01 describes how they identified many bat SARS-like CoV that bind human ACE2, and how they planned to collect many more (
https://twitter.com/jbloom_lab/status/1445780867427684363). (4/6)
This is why SARS-related CoVs pose genuine risk of zoonotic pandemics. It's also why collecting/manipulating them poses genuine risk of lab-associated pandemic. In general, the viruses that pose risks of natural & lab outbreaks are the same. (5/6)
This last fact is why we need to take zoonotic risk of potential pandemic viruses in nature seriously, but also consider very carefully risks of research on them in the lab (
https://mobile.twitter.com/jbloom_lab/status/1436522208545828869). (6/6)
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