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Was not aware of this article, but it seems like it centres on a particular paper that doesnt appear to describe gain of function, as there was no increase in pathogenesis, nor was this the intended goal. But as you allude to there are two separate considerations: the accountability of NIH if it was; the likelihood of such experiment being the origin of the virus.
They explicitly increase its pathogenesis. That's what the mutations they make are. They alter it to increase its binding affinity to human ACE2 receptors.