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Obviously, destroying vaccine-vulnerable strains of a virus will leave the vaccine-resistant ones to represent an increased fraction of the overall viral population. I'm asking, though, whether/how vaccination can allow a particular strain of a given virus to reproduce more than it would do without vaccination against another strain of the same virus, or to infect more hosts than it would infect without such vaccination.

If only vaccine-vulnerable strain A exists, might application of an anti-A vaccine somehow directly cause the mutation that creates resistant strain B? If so, how? Or are such mutations only random (in which case strain B might randomly arise even if the vaccine it was resistant to was never even invented)?

If strain A and strain B both already exist before any vaccine is developed, and then strain A is perfectly eradicated by a vaccine that strain B happens to perfectly resist, then of course strain B will remain - but will it actually benefit, in the sense of becoming able to increase its own population or its host population beyond what the respective count would have been without the anti-A vaccine? If so, by what mechanism?

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  • $\begingroup$ Mutations are random. Also, I think it would help clarify your question if you considered whether you are interested in virus "benefit" as absolute number of virus particles vs. percentage of total virus particles, particles in one individual vs. in a population, and at one point in time vs. dynamic change over time. Finally, "vaccine-vulnerable" is not yes/no, but a dynamic continuum involving many factors and portions of the virus lifecycle. $\endgroup$
    – Armand
    Jul 24, 2021 at 15:35
  • $\begingroup$ "absolute number of virus particles vs. percentage" - this should be clear already. "particles in one individual vs. in a population" - in a population (of potential and actual hosts), unless the other option is highly relevant in a way I'm not aware of. "at one point in time vs. dynamic change" - whatever is most relevant. I don't know much about this; that's why I'm asking. "'vaccine-vulnerable' is not yes/no" - in my A-and-B example it is, for the sake of simplicity. In reality: One case in which vulnerability of any sort helped a less-vulnerable mutant would suffice to answer the question. $\endgroup$
    – mjwach
    Jul 24, 2021 at 18:25
  • $\begingroup$ Antibodies/serum escape mutants are better studied (in-vitro and mice). Usually one escape mutation is not enough, the virus must accumulate 10 of these to be "resistant" and if each of these 10 mutations would have occurred anyway, the combination of the 10 would have been very unlikely without the selective pressure of the serum, making the 1st mutation rapidly fixed, then the 2nd and so on, with the neutralization by the serum decaying a bit each time. Change of selective pressure: some deleterious mutations becomes fit and conversely. $\endgroup$
    – reuns
    Jul 25, 2021 at 17:50
  • $\begingroup$ @reuns "the combination of the 10 would have been very unlikely without the selective pressure of the serum," - but why? How is the pressure exerted? If the mutations are random (meaning vaccination doesn't encourage or cause them), then vaccination shouldn't directly make that combo of 10 more or less likely to arise. Does it allow that rare mutant to flourish and become common by vanquishing the competition that would normally have kept the mutant in check? But in that case, HOW do viruses compete? Or is there some mechanism for application of pressure other than competition among viruses? $\endgroup$
    – mjwach
    Jul 25, 2021 at 21:29
  • $\begingroup$ Isn't it obvious? Mutation 1 is likely to arise without selective pressure but it will likely stay at a very low frequency and eventually disappear, with the selective pressure its frequency rapidly increases which gives a lot of chances for mutation 2 to appear in the background of mutation 1, and so on, the fit mutations accumulate. This process works as soon as the vaccine/serum pressure is not too high, so that the virus doesn't get extinct before finding the good combos of mutations. It's easier to study in lab with antibodies cocktail, decreasing the titer until the virus can proliferate $\endgroup$
    – reuns
    Jul 26, 2021 at 20:25

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OK, if you insist on the vaccine vulnerability being yes/no, then you've essentially got a situation where A and B are totally unrelated viruses. Here's a real-world situation:

Let's call A "COVID" and B "RSV". Before we had a COVID vaccine and during the lockdowns, RSV (respiratory syncytial virus), had dropped to very low levels because little kids were not mingling and transmitting it due to the school shut-downs, etc. This allowed the pool of non-RSV-exposed kids to grow and become a larger fraction of the population than normal. Once COVID vaccines began to be administered, society began to re-open and just recently, mid-2021, there have been many RSV outbreaks, with larger numbers of symptomatic individuals than typical, and more serious cases than normal.

In thinking about what you wrote a bit more, it seems like your "benefit to B from a vaccine against A" would require:

  1. Infection with A at least partially protects against later infection with B.
  2. The Anti-A vaccine provides less protection against infection with B than does previous infection with A.
  3. The Anti-A vaccine reduces the number of people who are infected with A before being exposed to B.

Items 1) and 3) together mean that the anti-A vaccine reduces the number of people infected with A, thus reducing the number of people at least partially protected against B because of earlier infection with A. (1) and (3) seem plausible to me.

However, the "benefit" for B would then require (2), that the anti-A vaccine provides less protection against B than does earlier infection with A. That is, those people who now are not infected by A would have less protection against B even after vaccination.

Although theoretically possible, this seems quite implausible to me, given the real-world data we've seen over the past year. What tests have been done seem to show that the Moderna and Pfizer vaccines provide better protection against variants than does previous infection with another variant.

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