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I can't speak for all the genes on that list, but I wouldn't go around knocking out FUT2 just yet. We don't know the full extent of biological roles for it, and the functionality is probably redundantly encoded in multiple genes too.

Specifically for viral interactions I reckon you'd be better off designing a small molecule inhibitor of viral binding via whatever lectin they have to whichever protein (or lipid for that matter) the sugar that FUT2 glycosylates is attached to. This allows for much more precise targeting of the undesired behaviour, rather than just chopping out the whole gene.

Agreed. I'm a non-secretor and I've benefited from not getting a norovirus when I really ought to have. But if such a valuable trait hasn't reached fixation in the population there's bound to be a reason. It also has a variety of effects on susceptibility to other diseases, some positive, some negative.


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