New Guy in Town

These graphs show the results of evolutionary experiments by Richard Lenski, in which a bacterial species ( e coli) has been evolving under constant conditions for many years: tens of thousands of generations.

These bacteria were not perfectly adapted to the experimental environment, and so there is selection for changes that allow them to do better in these conditions. Adaptive change is rapid at first and slows down with time, as the culture approaches an optimum phenotype. Fitness increases rather like the logarithm of time.

The probability of a beneficial mutation fixing is proportional to the advantage it confers. Large-effect beneficial mutations are more likely to fix and dominate the early phase. As the bacteria get closer to an optimum, the possible gain from a beneficial mutation is smaller, and so those smaller-effect beneficial mutations ( the only ones possible) are less likely to fix. Thus they take longer to fix (on average they need to occur many times before succeeding) and they also fix more slowly, since their growth advantage is small.

relevance: a new virus in humans is like the situation near the origin of graph B.  The virus is not yet close to an optimum, so change is fairly rapid – particularly if the virus is infecting vast numbers of people ( like covid-19) which greatly increases the number of copies of the virus and thus the chance of favorable mutations ( Fisherian acceleration). Favorable to the virus, that is.

An old virus in humans, say measles ( > 1000 years old)  is closer to an optimum: change is much slower.

It seems that most professional virologists are used to viruses that have been around for quite a while – understandable, since new viruses do not sweep through the human race every year.

You could have predicted the emergence of new higher-transmission variants of covid-19 from this theoretical perspective. I did, arguablywrong did, probably others have as well. But virologists did not.

 

 

 

 

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48 Responses to New Guy in Town

  1. cameron232 says:

    I apologize for threadjacking. Monozygotic twins are not identical and, as a consequence, heritability of g may be underestimated?

    Does this make sense?

    http://evoandproud.blogspot.com/2021/01/are-identical-twins-really-identical.html

  2. teageegeepea says:

    I’m just seeing “image.png”. It looks like the image source is under google mail.

  3. jbbigf says:

    If measles is optimal’, why doesn’t everyone have it?

  4. Robert says:

    Any idea why Influenza hasn’t evolved to spread easier like Covid is?

  5. The other thing that was interesting about that paper was the discussion of point mutations vs. structural rearrangements. Point mutations are much more common, while structural rearrangements are much rarer, but can cause much larger swings in phenotype. They pointed out particularly the observed evolution of the ability of E. coli to survive on citrate rather than glucose, which involved moving the whole damn citrate importer gene over to a different promoter.

    The other thing of interest is that hypermutability mutations – things which make mutations more common – are fairly likely to evolve when the bug is far from its local equilibrium. Because any strain that happens to have a broken repair system is also more likely to pick up one of the ubiquitous beneficial mutations. I was, frankly, rather terrified that this had happened with the UK strain, but it luckily doesn’t look like it.

  6. For comparison, we’re ~70 generations of replication or so into Wuflu as a novel human disease. There’s a lot of room at the top.

  7. John Massey says:

    I hear things are already pretty rough in Brussels – but they can always get a lot rougher: https://www.youtube.com/watch?v=C5tBuPTn3Mk

  8. John Massey says:

    While I’m playing silly bastards, only marginally off topic – who knew that Ariana Grande can belly dance like Shakira? Sorry about the subtitles.

  9. sonOfRekab says:

    Makes sense
    But why does the flue keep comming back in a new form each year, do we know how old it is?

  10. josh says:

    So how long can I realistically expect to be protected by my (pfizer) vaccination?

    • mapman says:

      It’s a statistical thing but if your response was at or above the average titers that were seen in the trials (those tended to be higher than average in the convalescent sera), you should expect a minimum of 6 month. Beyond that, nobody knows for sure (could easily be a full year) but chances are really good that if 1 year from now you’ll still get infected, you will be either asymptomatic or it will be like a regular cold at worst.

  11. swampr says:

    Greg, have you seen this paper comparing the adaptation of SARS2 vs SARS1? One of the authors is the most prominent lab-leak proponent. It’s been stuck in peer review since May and I’m curious if their method is legitimate. Related to your point but in the opposite direction since it’s on a short timescale.
    https://www.biorxiv.org/content/10.1101/2020.05.01.073262v1.full

    • Frau Katze says:

      China will never admit it.

    • John Massey says:

      So that is what is burning Alina Chan’s arse so badly – she can’t get her paper through peer review.

      • John Massey says:

        “Now rewritten and under peer review at a 2nd journal.” Uh huh.

      • swampr says:

        I just want to know what experts think of her paper. The only extensive commentary I found is this back and forth with a “phylogenomicist”. He says pretty clearly elsewhere that a lab leak is quite plausible but had serious reservations about the paper in its initial form. Like you’re jumping to conclusions, but somewhat interesting. Here’s what to look at it you want to make a real case. She says since then that they’ve reworked it based on feedback. He doesn’t seem to have revisited it.

        https://mobile.twitter.com/phylogenomics/status/1262130860435763200

      • John Massey says:

        Well, as no experts have responded, I will comment on one thing;
        “Several reports have noted that SARS-CoV-2 appears genetically stable and not under much pressure to adapt, which bodes well for diagnostics, vaccine, and therapeutics development.”
        Given how many mutations there are now which are more contagious (one in the UK, one in South Africa, one in Brazil and two in Japan, and I am starting to lose count), and which might yet prove to evade vaccines, that statement should really be revisited, shouldn’t it?

        I mean, far from being ‘genetically stable’, having passed through many millions of people, it is mutating rapidly to become even more infectious in multiple different places. And it is under no selective pressure at all to become less virulent. In fact, it could probably afford at this point to become more virulent, and maybe starting to kill some young folks, although there is no selective pressure for it to do that either.

      • John Massey says:

        Of course, she has a reason for trying to push the line that it is perfectly adapted to humans, but Eisen wasn’t going to let her get away with that – he at least is an objective scientist, even if she isn’t.

        If she wants to keep up the appearance of being an objective scientist, she should probably avoid interspersing her tweets with ideological propaganda.

  12. Coagulopath says:

    It throws into light why the Old World diseases were so bad when they hit America.

    From the virus’s perspective, they had all the benefits of a old disease (lots of time to reach their optimum), and all the benefits of a new disease (a huge population with basically zero immunity). It was the best of both worlds.

  13. Luke Lea says:

    Greg, could you give us a general overview of where you think we are with this virus right now and where you think it is going? I know you did early on, but by now most discussions are so deep in the weeds that us poor layman are lost.

  14. Mike-SMO says:

    In reference to the Kung Flu:

    1) it is likely that a mutation in the “infectuous spike” of the virus allowed it to jump into humans. All the current mutations seem to involve secondary effects. If the RNA “vaccine” targets the spike (or some part of it), any mutation that allows the virus to escape the immune attack also makes it unable to use the Angiotensin-II enzyme/receptor to attack the vital cells in the lungs and vasular bed. The RNA “vaccine” don’t care what the virus is “wearing”.

    2) The Corona virus has been tracked by a whole series of mutations. As long as the lethality of the infection does not significantly change due to new mutations, so what? In a world with Interstate highways and air travel “herd immunity” is irrelevant, although useful. An effective vaccine is the most relevant thing for the old/sickly potential victims, although it doesn’t give perfect protection for all. I am more interested in the medical and or genetic characteristics of those, of all ages, who die quickly from the Corona infection. There is something “useful” going on there.

    3) Laboratory vs. Bird Shit. (That is a technical term.)
    China has been generating new and horrific diseases for centuries. It makes sense to fund research in that pest hole. Apparently both the U.S. and France have done so. High threat labs are a “bear” to operate and to work in. A leak would be no surprise especially in the corruptocracy of China. E.g. A lab director gets his position since he is a pal of the local party hack. The director hires his stupid son-in-law to clean cages. A “leak” is inevitable, because no one is going to “tell”.

    The virus probably originated in southern China where a mixture of farm animals, raised in the open, eat and crap in the same rice paddies as do the bats and weird creatures from the near-by mountains, all in close proximity to a billion or so humans in the cities. “Civit Cats” crap coffee beans, but what is a “pangolin”? [Looks like a failed first attempt at an Armadillo.] The rice paddy party includes migrating wild bird species who mix with the migrating birds of most of the world in Siberia and Alaska. New diseases appear under major migratory fly ways. MERS in the Gulf, Covid-19 in Iran. Israel has a problem with Corona in their chicken flocks. “Bird Flu” appeared in Mexico. Way back, the first cases of the “Spanish Flu” (1917 as I recall) appeared in Kansas, where there was too small of a population to support a major outbreak as occurred in Europe where domestic ducks and geese were used to feed allied troops, who were living in tent ghettos. The “Pig Ebola” spread rapidly all over China, even though pigs can’t ride motorcycles to visit their friends. Use care when cleaning your windshield or yard furniture.

    I don’t have the links at hand, but EU data showed spring increases in COVID-19 deaths only in places that also had “normal” spring surges in “seasonal” Flu deaths. That is, both occurred in the same areas, in southern and western Europe which are nesting or transit locations for migrating birds. The seasonality of the Flu is normally attributed to bad weather and HVAC but both the Flu and COVID-19 surges occur after the Fall bird migrations of birds leaving the Arctic party. Italy got both the bird and Chinese factory worker migrations. Bummer. In summary, Bird crap kills people in China and everywhere else that is covered in birdy poop. It is just a theory. Incoming! We have “lazy” “Canadian” geese population that turns a sloped lawn into a “slide for life”. No one checks for migrating visitors.

    By the way, plague in western North America probably came from China via the rats and fleas on the ships bringing tea and railroad laborers. COVID-19 is just probably the latest “gift” from Asia. The CCP made COVID-19 worse in Italy, but I don’t think that humans had to do a thing to make this happen, eventually. All the wings are not from Boeing and Airbus.

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