Then after a few hundred years, the human population will have undergone enough selection that all the bad HLA alleles that make T-cell responses difficult are low in the population and all the formerly rare ACE2 alleles are widespread. Here, check out these papers:
Looking at signatures of natural selection in the human population, by FAR some of the strongest signals in the past few tens of thousands of years is proteins that interact with viral proteins—the HLA alleles and all the parts of the interferon response and everything else that all those tricksy accessory proteins sequester and alter.
This is nothing new. We just have somehow decided that we expect better.
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As for other things:
The virus apparently has a mutation rate which is on the high end, unexpectedly large rate of mutation. This makes the vaccine less probable. How much less? No idea.
This is simply not true. Coronaviruses actually proofread their polymerases unlike almost all RNA viruses. The only interesting mutations I am aware of in the current outbreak is two independent origins of a particular missense mutation away from the receptor-binding-domain of the spike protein (that thus dont affect neutralizing antibodies), and a few strains that have up and LOST whole accessory proteins that are part of how the virus evades the innate immune response (because they are so damn good at evading it in humans because the bat response is so absurdly fast that they don’t need half of what they have).
Following the vaccine development scene, I am actually absurdly optimistic. All the stuff entering human studies are basically just repurposing already-researched SARS and MERS vaccines that work in monkeys, and swapping out the sequence. The preliminary data is already coming in in these animals and is good.
Thanks for those links. I’ll need time to read properly.
I’ve wondered for a while about the influence of viruses on evolution (just looking at the effects of something like Zika virus for a start) or genomes picking up “new DNA” from RNA templates etc.…
It is mostly just retroviruses that wind up entering the genomes of their hosts. RNA viruses leave a very different imprint: high rates of evolution of the proteins that their proteins interact with, as they race to deactivate their hosts immune responses and their hosts race to deactivate or evade the viral proteins.
There is also a constant, diversifying selection on the components of the immune system (HLA/MHC) that display viral proteins from within cells on cell surfaces for the immune system to be sensitized against. Viruses always evolve to take better advantage of the most common of these alleles, and the rarest of these genes are always selected for in populations as result. The end result is what is called ‘balancing selection’, where rare things become more common and common things become less common leading to the maintenance of great diversity. This is why tissue typing for transplants is so difficult—there is such immune system diversity that most people don’t have the same alleles at these loci as each other. Of course, if something new enters the population that a subset of these alleles isn’t great against, that set of alleles will become less common over time.
Then after a few hundred years, the human population will have undergone enough selection that all the bad HLA alleles that make T-cell responses difficult are low in the population and all the formerly rare ACE2 alleles are widespread. Here, check out these papers:
https://elifesciences.org/articles/12469
https://www.biorxiv.org/content/10.1101/2020.03.18.997346v1.full
Looking at signatures of natural selection in the human population, by FAR some of the strongest signals in the past few tens of thousands of years is proteins that interact with viral proteins—the HLA alleles and all the parts of the interferon response and everything else that all those tricksy accessory proteins sequester and alter.
This is nothing new. We just have somehow decided that we expect better.
------
As for other things:
This is simply not true. Coronaviruses actually proofread their polymerases unlike almost all RNA viruses. The only interesting mutations I am aware of in the current outbreak is two independent origins of a particular missense mutation away from the receptor-binding-domain of the spike protein (that thus dont affect neutralizing antibodies), and a few strains that have up and LOST whole accessory proteins that are part of how the virus evades the innate immune response (because they are so damn good at evading it in humans because the bat response is so absurdly fast that they don’t need half of what they have).
Following the vaccine development scene, I am actually absurdly optimistic. All the stuff entering human studies are basically just repurposing already-researched SARS and MERS vaccines that work in monkeys, and swapping out the sequence. The preliminary data is already coming in in these animals and is good.
Thanks for those links. I’ll need time to read properly.
I’ve wondered for a while about the influence of viruses on evolution (just looking at the effects of something like Zika virus for a start) or genomes picking up “new DNA” from RNA templates etc.…
It is mostly just retroviruses that wind up entering the genomes of their hosts. RNA viruses leave a very different imprint: high rates of evolution of the proteins that their proteins interact with, as they race to deactivate their hosts immune responses and their hosts race to deactivate or evade the viral proteins.
There is also a constant, diversifying selection on the components of the immune system (HLA/MHC) that display viral proteins from within cells on cell surfaces for the immune system to be sensitized against. Viruses always evolve to take better advantage of the most common of these alleles, and the rarest of these genes are always selected for in populations as result. The end result is what is called ‘balancing selection’, where rare things become more common and common things become less common leading to the maintenance of great diversity. This is why tissue typing for transplants is so difficult—there is such immune system diversity that most people don’t have the same alleles at these loci as each other. Of course, if something new enters the population that a subset of these alleles isn’t great against, that set of alleles will become less common over time.