:sadness-abysmal:

    • CheGueBeara [he/him]
      ·
      2 years ago

      They do, but it's just on average and can be something that happens on the order of decades.

      They essentially take a biased random walk, with that bias being towards less severe immune response, itself responsible for most of the impacts of disease.

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

        They don't always. HIV is one of the most rapidly mutating virus in history and has not become less virulent.

        • CheGueBeara [he/him]
          ·
          2 years ago

          That's true, though HIV is a bit special in its relationship with the immune system and how it causes disease. It does have some direct and serious symptoms related to inflammation, which is the classic way in which diseases cause damage, but the major impact of HIV on people's bodies and its deadlines is in destroying the immune system itself, namely T cells. This means that the "usual" selective pressures are much weaker and could even be the opposite when it comes to AIDS.

          I should note that I don't know the evolutionary history of HIV's health impacts outside of destroying the immune system. For example, it causes brain inflammation and has impacts on cognition, but I have no idea if that has gotten worse, better, or stayed the same over time.

          Thanks for pointing this out, though! It's a very good thing to keep in mind. The specifics of the disease really do matter, as do timelines, and the trend with SARS-CoV-2 doesn't make me optimistic about timelines.

          • MedicareForSome [none/use name]
            ·
            2 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
              2 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.

      • crime [she/her, any]
        ·
        edit-2
        2 years ago

        Nothing says they have to. As long as a virus can infect new hosts quickly and efficiently there's no problem if it kills the one it's currently in.

        • CheGueBeara [he/him]
          ·
          2 years ago

          They don't have to, but there's nearly always a selective pressure to because of the coupling between immune escape and not causing horrible symptoms, which are themselves usually the immune system's response. Example: COVID doesn't kill the lungs through the virus itself screwing them up, but because it infected them rapidly and invokes an immune response there, creating inflammation and scar tissue from associated damage.

          The reason it's a random walk is exactly what you're saying, though. A more severe variant can take over so long as it's better at spreading, which isn't solely a function of avoiding immune response, and hasn't exhausted its hosts. The last two variants that took over produce way higher viral loads and are still quite severe, for example.

          A virus can also get less severe for a while, then get displaced by a more severe variant. Imagine, for example, if the next dominant variant were noticeably less severe and didn't cause permanent lung damage. Libs would declare victory (they're already trying to with omicron copium), but the next variant after that to take over could be more virulent simply because everyone is now more immune to the less severe one and not our huge backlog of shitty variants (let alone new ones).

          And this stuff can take a very long time.

          Just wanna stress that this is a real tendency in diseases and widely recognized in microbiology and people who study the evolution of infectious diseases but also it's a really bad excuse for thinking things will be fine on any acceptable timelinr. That excuse is also copium spread by a ruling class that is running the people through a COVID meat grinder and the people themselves who see that help is not coming and find this idea appealing.