3 ms·

> cov2 was a bat virus -- so it needed an intermediate mammal host with human-like ace2 receptors to spread to humans. My understanding is that bats like the

> cov2 was a bat virus -- so it needed an intermediate mammal host with human-like ace2 receptors to spread to humans. My understanding is that bats like the chinese horseshoe have perfectly suitable ACE2 receptors for getting infected by sars-cov-2 as-is, and that the main reason for wanting an intermediate host is to explain how the virus got in contact with humans because humans don't really interface physically with bats, but I'm totally out of my depths here. The article linked below makes it sound like the virus can infect a wide variety of mammals, including bats and humans, with or without the now famous furin cleavage site, so it doesn't seem like the smoking gun lab-leak proponents like to brandish it as. https://www.news-medical.net/news/20200420/ACE2-receptor-expression-by-SARS-CoV-2-across-different-animal-species.aspx https://www.news-medical.net/news/20200420/ACE2-receptor-exp...

mikeyouse 5y ago
This closely mirrors my probabilities; https://medium.com/advances-in-biological-science/explained-the-hard-evidence-why-the-sars-cov-2-genome-was-not-engineered-and-unlikely-leaked-f3d6fbb10ff9 https://medium.com/advances-in-biological-science/explained-... It's extremely unlikely that the jump was from bats -> humans just based on how 'optimized' the ACE2 binding and furin cleavage sites are. It's theoretically possible that it happened at some time in the past, and then serial passage in humans led to the more 'optimized' virus but that seems pretty unlikely too.
- tripletao 5y ago
  Are you aware of BANAL-20-52's spike? That's a bat virus, and it's only 16 AA substitutions (plus no FCS) away from SARS-CoV-2: https://twitter.com/jbloom_lab/status/1440309655087902720?lang=en https://twitter.com/jbloom_lab/status/1440309655087902720?la... I've seen no explanation for why the spike of a bat virus would be so well-adapted to human ACE2, but apparently that one is. That's an argument against the need for an intermediate host, whether that host is natural (e.g. a non-bat wild animal) or not (e.g. hACE2 mice in the lab).

mikeyouse 5y ago

This closely mirrors my probabilities; https://medium.com/advances-in-biological-science/explained-the-hard-evidence-why-the-sars-cov-2-genome-was-not-engineered-and-unlikely-leaked-f3d6fbb10ff9 https://medium.com/advances-in-biological-science/explained-... It's extremely unlikely that the jump was from bats -> humans just based on how 'optimized' the ACE2 binding and furin cleavage sites are. It's theoretically possible that it happened at some time in the past, and then serial passage in humans led to the more 'optimized' virus but that seems pretty unlikely too.

tripletao 5y ago
Are you aware of BANAL-20-52's spike? That's a bat virus, and it's only 16 AA substitutions (plus no FCS) away from SARS-CoV-2: https://twitter.com/jbloom_lab/status/1440309655087902720?lang=en https://twitter.com/jbloom_lab/status/1440309655087902720?la... I've seen no explanation for why the spike of a bat virus would be so well-adapted to human ACE2, but apparently that one is. That's an argument against the need for an intermediate host, whether that host is natural (e.g. a non-bat wild animal) or not (e.g. hACE2 mice in the lab).