Can anyone with more knowledge on this topic than me (I’m no expert) assuage my fears: by giving human populations such artificial resistances (non-live vaccines) we run the risk of selecting for viruses that are even harder for even our own immune systems to detect and destroy. Current Covid strains don’t seem all that bad, basically everyone I know has been infected now. Might we run the risk of making things worse…
Evolution is climbing mount improbable. And natural selection (even in the face of in this case intelligently designed selectors) funnels organisms into potential dead ends which they can’t evolve out of - they’ve gone up the ‘north face’ and in order to reach fitness in the face of their selectors, they actually need to be on a completely different mountain. An antibody that dead ends all current evolutionary trends…
> Once the virus has bound to ACE2, it must complete a final step: fusing its outer membrane with the membrane of our cells. This throws the door open to infection. Using a novel live-cell imaging platform, Alex Kreutzberger, HMS instructor in pediatrics at Boston Children’s, and Tomas Kirchhausen, professor of cell biology in the Blavatnik Institute at HMS and professor of pediatrics at Boston Children’s, showed that SP1-77 blocks this step.
> “SP1-77 binds the spike protein at a site that so far has not been mutated in any variant, and it neutralizes these variants by a novel mechanism,” noted Kirchhausen. “These properties may contribute to its broad and potent activity.”
Questions:
* If mutations at this site are possible, how would this be an evolutionary deadens in a way that the current evolutionary dynamics of the virus are not?
* Surely a lack of mutations at this site, on their face, imply only that there is no evolutionary pressure on the site and its phenotypes, and, that mutations at this site are as viable as anywhere else?
* Or, is it possible that the lack of mutations (presuming that this is very accurate) indicates an evolutionary pressure to maintain functionality that is sensitive to failure due to even minor mutations or deviations in functionality?