People who don’t believe in evolution are idiots, but the coronavirus cannot evolve

One evergreen fun activity for American Democrats is saying that Republicans are idiots because they purportedly don’t believe in the theory of evolution. (As Democrats generally live in cities that are devoid of Republicans, it is unclear how Democrats would know what Republicans actually do and don’t believe.)

The same folks are also saying that forcing every American to be injected with a COVID-19 vaccine will end the frightening coronaplague that has lead to coronapanic and shutdown.

Are these points of view consistent?

Why can’t the coronavirus evolve its way around the vaccine, in the same way that influenza evolves to defy our vaccination attempts? And why can’t it evolve to spread even among a mostly masked-and-cowering-Clorox-armed population?

In the early months of coronascience, we were told that the virus was mutating more gradually than influenza. And presumably the most successful mutations will be less deadly (killing one’s host is a suboptimal strategy for a virus).

(Why does this matter? Shutdowns, mask wars, school closures, etc. make sense only if you think coronavirus is a temporary one-and-done phenomenon. If coronavirus will be an influenza-style permanent companion to the 8 billion humans on Planet Earth then it doesn’t make sense to do anything now that we aren’t willing and able to do for the next 50 years.)

Should we schedule a reminder to look at this in February 2022? What’s a threshold of cases and/or COVID-19-tagged deaths that we should use from, say, September 2022-February 2022 in the U.S. to declare vaccine victory or vaccine disappointment?

Update: A Facebook friend updated his profile picture to say “When It’s My Turn, I’m Getting Vaccinated! Goodbye COVID”:

In other words, he’s denying the possibility of the virus evolving its way around the vaccine, as well as assuming that the vaccine prevents transmission (as yet unknown) and that the vaccine will prevent deaths among the old/sick (also as yet unknown because never tested). His tagline is “Yes: Facts,Equality,Justice,Freedom, Intelligence,Confidence. No: Ignorance,Intolerance,Corruption.” so presumably this is an “intelligent” perspective. (My Facebook tagline: “I like to do everything in the dumbest way imaginable.”)

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12 thoughts on “People who don’t believe in evolution are idiots, but the coronavirus cannot evolve

  1. Letting the virus reproduce and mutate among the general population with a “let it rip” strategy certainly gives the virus more opportunity to evolve!

    To the extent it evolves beyond the vaccine or other current measures before it can be irradiated—oops!

    • ANON: I think your comment requires an assumption that humans are in charge of the coronavirus and viruses in general. It is for us to decide whether or not the virus will reproduce.

    • China decided to not let the virus continue reproducing (or at least, not nearly on the scale the US is allowing it to). Unfortunately, if you’ve seen the movie American Factory, you’ll realize that people in China are smarter and harder-working than Americans so we can’t expect the same quality of results here.

    • Philg: Virus will reproduce and evolve no matter what. Humans not in charge of that.

      Human behavior can influence the rate of reproduction, thus the population size of the virus as a function of time. ( example dumb thing people say: “Masks either work or they don’t.” Not binary, masks work to reduce rate significantly. )

      The smaller the virus population size over time, the less opportunity for the virus to reproduce and mutate.

      The less opportunity for reproduction and mutation, the smaller the chance the virus will mutate into a variant that is more optimized to spread easier and isn’t hindered by current vaccine.

      Easier to make a smaller virus population to go extinct (or nearly so) than a big virus population. See China as an example as noted by Ryan.

  2. My understanding is that we may need shots every fall (like we get for the flu) because of the constant mutations/strains. Even Fauci says it’s never going away (https://www.cnbc.com/2020/07/22/dr-anthony-fauci-warns-the-coronavirus-wont-ever-be-totally-eradicated.html). Why I think Sweden’s approach (maybe Anders’s thinking) has a lot of merit.

    Maybe after a year or so, the COVID-19-tagged deaths will just vanish into the CDC stats and be absorbed by (calculated) flu deaths / year. And we will be fascinated with or bombarded with something else.

  3. I thought it was well accepted we’ll all need a new COVID-19 vaccine every year forevermore. It will become substantially less exciting than the current vaccination schedule, I am sure of that.

    • Federico: But if the COVID-19 vaccine works only as well as the flu vaccine, there will still be enough COVID-19 deaths to justify a permanent shutdown (since COVID-19 is deadlier than the typical flu).

    • I don’t know about a permanent shutdown, but permanent COVID would result in a massive talent exodus from the US to places like China, Taiwan, Singapore, New Zealand, and Australia. If you’re not old enough to be at serious risk from COVID now, you hopefully will be eventually. Who wants to grow old in a country that doesn’t give a shit about old people?

    • Phil, how? if a vaccine covers ~90% of the population, how can the mortality stay the same? plus a vaccine will select for mutations in the virus, and our reaction to them will further select less dangerous strains.

    • Federico: As noted in https://philip.greenspun.com/blog/2020/12/27/if-covid-19-vaccines-werent-tested-on-likely-covid-19-victims-how-do-we-know-that-they-will-reduce-covid-19-deaths/ , we can hope that the vaccine will reduce mortality, but we have no evidence for that from the trial. Hardly anyone in the Moderna trial died, either in the vaccine or placebo group (15,000ish people each). Nobody in either group died from COVID-19. No vaccine has ever been tested on the old/sick people who have died in significant numbers from COVID-19.

      Similarly, the trials didn’t test for asymptomatic infection and transmission. We can hope, but don’t know if vaccination will help.

      Also… how many deaths is enough to justify a shutdown? Sweden has a lower all-cause death rate than it did in 2010. Nonetheless, it would be easy to find people in Sweden who advocate for shutting down. Unless the vaccine can prevent 100% of COVID-19 deaths, I suspect we will not run out of mask-and-shutdown advocates.

  4. If I understand it correctly, the Moderna “vaccine” is actually a synthetic virus that prompts protein production, similarly to a natural virus, but without the self replication.

    https://www.modernatx.com/mrna-technology/mrna-platform-enabling-drug-discovery-development

    One wonders what “life” is as it pertains to a virus. We can appreciate that bacteria are separate organsims that use human bodies as a habitat, sometimes as necessary symbiotes, as in the digestive track.. But a virus is so minimal and dependant on its host cells for reproduction that considering it as a separate organism is insufficient.

    How did viruses, as a life form, come into being? What is their evolutionary history? What is the life cycle of a virus? How is the evolutionary concept different in manifestation from viruses to bacteria to man? What roll do viruses play in the broader ecosystem? Do they act as a predator in keeping down population levels?

    These are the type of basic questions one should have a coherent answer to before tackling a practical problems in a philosophic matter.

    I have left out questions relating to the human immune system and how it learns and fights disease. To include such questions about a coronavirus variant that is benign to the vast majority of people would only further confuse the issue at hand.

  5. An antibody binds to an “epitope”, which is an exposed portion of a protein that the immune system somehow recognized as foreign. If you’re fighting the virus with a single kind of antibody, it binds to a single epitope, and any mutation in the virus that changes that epitope will make the antibody useless.

    This is obviously a concern for monoclonal antibodies therapies, which are just huge numbers of copies of the same antibody. That’s why Regeneron doesn’t sell a single monoclonal antibody, but a “cocktail” of 2 antibodies: even if the virus might evolve to escape one of the antibodies, it’s highly unlikely that it will evolve to escape both (unless everybody starts taking Regeneron’s cocktail preventatively).

    When it comes to vaccines, however, most of the COVID-19 vaccines work by delivering/producing many copies of the virus spike protein inside your body, and letting your immune system produce whatever antibodies it wants. The advantage is that the spike protein is huge (I’ve heard something about 20 epitopes, but don’t quote me on that). The immune system is very unlikely to produce antibodies for all the epitopes, and even if it did, most of them would not bind very well to the virus. But the antibodies in the population would be diverse enough that the virus is highly unlikely to evade all of them.

    Coronaviruses don’t evolve very fast, in fact they have a proofreading mechanism [1] to slow down evolution. You can get infected again with the same coronavirus, but most of the time it’s not because the virus has evolved, it’s because you never had good antibodies for it in the first place. There is speculation that a protease (enzyme that cuts down proteins) produced by many coronaviruses also suppresses the immune response [2]. If that’s true, the immunity from spike-only vaccines should be even better compared to a normal infection.

    The flu viruses are the opposite: not only they don’t have a proofreading mechanism, but their RNA is split into multiple segments, so 2 flu viruses that meet in the same cell can mix and match. This can even happen if the host would normally be a dead end for one of the viruses, allowing continuous “horizontal” gene transfer between the human flu viruses and the avian/pig flu viruses.

    [1]: https://pubmed.ncbi.nlm.nih.gov/21593585/
    [2]: https://pubmed.ncbi.nlm.nih.gov/25481026/

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