I don’t know that it’s entirely possible to seperate out adaptation of the human population from adaptation of the infecting viruses. Certainly, the virulence of said viruses (or in the case of bubonic plague, bacteria) in nonconditioned populations is much greater, but within experienced populations the less virulent (but more pervasive) strains will tends to thrive over those which are too destructive. Adaptation between species (as I’m sure you’re aware) is never a one-way street; the Red Queen has to adapt to run faster just as her pursuer does.
Existing viruses and bacteria, barring some unlikely mutation that makes them more virulent, will tend to become less benign in effect, thus triggering less of a response that limits transmission. A chest cold that lays someone out for a week is less likely to be widely communicated than a sinus infection that causes a mild nasal drip and frequent sneezing.
Regarding the jumping of infections between animals and human populations, there may be something of a misconceptualization here. It’s not that an infectious organism–say, a virus–is transmitted from lifestock to a human, fully adapted, but rather that the organism which has arisen in, say, a cow, demonstrates some viability in humans. It replicates and is transmitted back to lifestock, in slightly greater proportion than before. It then jumps back to a person, develops again, et cetera, with mutation and adaptive selection enhancing its ability to exist and replicate in human populations. Eventually (or perhaps quite rapidly) it becomes highly virulent, especially if communicated to a genetically unadapted population of humans, and from there proliferates. It’s likely that infectious strains jump back and forth between humans and husbanded animals quite regularly, especially prior to effective sanitation, preventative inoculation, and the processing of animal food products to remove harmful bacteria (pasturization, thermal sterilization, refrigeration, irradiation, et cetera).
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