:sadness-abysmal:

  • MedicareForSome [none/use name]
    ·
    3 years ago

    Yeah SARS-CoV-2 is a slow mutating virus because it codes for its own replication proteins and therefore has an error-checking protein for its genome called NSP14. That's also why the virus is resistant to traditional nucleoside analog based antiviral drugs. To my knowledge, all coronaviruses are like that.

    The idea that viruses evolve to reach equilibrium with the host is only really true in the most literal sense. As in, a virus that wipes out 100% of the population will cease to exist because there will be no more hosts. There really isn't that much evolutionary pressure because it really doesn't kill that many people relative to the number of infected.

    The idea that as long as we keep feeding the virus, it will eventually go away is not really scientific.

    The "law of declining virulence" was written by Theobald Smith in the 1800s. Here is a mildly informative article about it from the other day: https://abcnews.go.com/Health/debunking-idea-viruses-evolve-virulent/story?id=82052581

    The necessity of disease eradication is pretty modern. Historically, If a new virus came out and killed an entire village it would stop there just because there was no plane to get on. Small pox also had to be eradicated, it never lost its virulence. Rabies hasn't, neither has measles or polio.

    If the same mutation causes more people to die but also causes faster spread, that mutation will dominate. It's basically hoping for a happy coincidence. I hope for these types of coincidences but they're not inevitable and it could just as easily get worse.

    • CheGueBeara [he/him]
      ·
      edit-2
      3 years ago

      I think the best way to communicate what I mean is that I'm describing trade-off theory, which is mainstream science taught in universities everywhere, and not avirulence theory, which is that 1800s theory. I scrounged around trying to find a good explanation from a university course but nothing very good popped up. This review in Cell from 2017 is pretty good: http://hedricklab.ucsd.edu/documents/Hedrick-CellReviews-2017.pdf

      There are more detailed examples and explanations that elaborate on the mechanisms of decreased severity. For example, secific immune responses are often what cause the most recognized damage (this is true of SARS-CoV-2) and the same mechanisms that improve transmissibility are often about preventing those exact responses, making the virus both less severe and more transmittable. So long as those strains compete for hosts, the trend will hold. Luckily, the spike protein seems pretty specific for ACE2 and it's the major place where competition would evolve away.

      With that in mind, it's very important to emphasize that this is still a random walk, that it happens on evolutionary time, and that the pathogen has more space to explore transmissibility when it's just jumped from a zoonotic host, so (1) things can get worse before they get better, (2) things can get better and then get bad again, and (3) it could take years, decades for this trend to matter.

      One thing that I should probably focus on more is why we're even talking about this. It's not because we're all suddenly interested in pathogen-host evolutionary ecology! It's because the capitalist ruling class has prevented an actual eradication or even control response, so this is their propagandized copium: maybe the virus will fix itself. And people latch onto it because they know help isn't coming and they want the pandemic to be over, they want to be safe, they want to return to some level of normalcy. These are false hopes over the timeframes they're hoping for given the trajectories of SARS-CoV-2 variants. We should be pushing back on this within and through our socialist parties.