Antibiotic selection does not have the same dynamics as viral evolution does. This graphic demonstrates a good example as to the epitope coverage across S by b

Antibiotic selection does not have the same dynamics as viral evolution does. This graphic demonstrates a good example as to the epitope coverage across S by both B-cells and T-cells: https://www.medrxiv.org/content/medrxiv/early/2021/07/05/2021.07.01.21259833/F7.large.jpg https://www.medrxiv.org/content/medrxiv/early/2021/07/05/202... You would need to have a variant that selects past all of the epitope coverage of both B/T-cell and bypasses affinity maturation too. NTD and RBD already has great coverage, but the rest of the pre-fusion spike confirmation used in vaccines these days has even more coverage than just with RBD alone. I think that's why BNT162b1 failed, as it was a mRNA encoded receptor binding domain only. Given how large the breadth (as in epitope coverage) already is in RBD alone, you would most likely disrupt ACE2 receptor binding too at the same time if there was a such a massive change all at once to render a vaccine useless. If you managed to achieve an evolution rate of 250+ AA substitutions extremely quickly, all in one fell swoop, I’d have much much bigger concerns. A lot of the variants these days select for escape for RBD class 1 and 2 nAbs, even Mu as of now (R346K is in this weird overlap between the different classes as per the Barnes classification). You may want to see the following: https://www.nature.com/articles/s41579-021-00573-0 https://www.nature.com/articles/s41579-021-00573-0 https://www.nature.com/articles/s41586-020-2852-1 https://www.nature.com/articles/s41586-020-2852-1 https://www.science.org/doi/full/10.1126/science.abf9302 https://www.science.org/doi/full/10.1126/science.abf9302 I think I read some others, but I'll have to dig through my browser history more.