[mleonhard]

In the article, the authors say that, in 2015, US researchers created a chimeric virus from a bat coronavirus to infect mice lung cells. They tested the virus on human lung cells and predicted that it would be very dangerous to humans. They stopped doing research on it because it would break the US rules against making human viruses more powerful. They were working with virus researchers from Wuhan. The authors conjecture that the Wuhan researchers used the same techniques and made Sars-cov-2 and it accidentally got out.

[sudosysgen]

The issue is that SARS-CoV-2 is much, much less powerful. So that doesn't really follow.

[SomeoneFromCA]

Compared to what? Not much is known how powerful that chimeric virus was compared to CoV-2. Could please elaborate where did you get that notion from&

[tomp]

What do you mean by this? I heard that it has incredible affinity to ACE receptors, which is why it sprrads so quickly (combined with asymptomatic infection)

[sudosysgen]

Yes, it binds to ACE2 receptors more strongly, but once you're infected it's about one order of magnitude less severe.

To note, receptor affinity is not the only mechanism by which infectivity is modulated. You would already expect that a virus that is ten times less severe would spread more easily, and SARS was already able to spread efficiently through air at great distances, so it seems likely that me that receptor affinity is stronger but that other mechanism are weaker. This would explain the fact that it is less severe and not much more infectious.