By which I mean variants that do the expected thing where mutations increase transmissibility but decrease virulence?
The logic of natural selection would tell us those should be the much more common kinds of variants as they should increase the changes of newer generations of virus surviving to reproduce.
It’s strange to me that all of the variants discussed have both increased transmissibility and virulence. It seems anti-Darwinian.
If there are thousands of VOIs (variants of indifference), which you might predict for every VOC, could that not have an effect on the overall statistics? More people get less virulent VOIs and some immunity?
Although it is widely held by biologists that there is a tradeoff between infectiousness and virulence, people (eg, Paul Ewald) who actually study the evolution of virulence say the opposite, both in theory and data. In the case of sars2, it is overdetermined: death is due to immune overreaction, after the window of selection is over.
Does he have anything to say about the case of sars-Cov-2 specifically?
On one hand, yes it seems like there’s something like antagonistic pleiotropy here where most of the transmission is done before the “acute phase” (the time when your o2 sat drops and you go to the ER, there’s probably a better term for that I’m just not sure what it is).
But we’re also applying non-trivial selection pressure via lockdowns and other precautions, and if sars-Cov-2 would stop killing people and just give them a runny nose we would stop and it could reproduce more. I’m just not certain why that isn’t have more of an effect.
Is anyone tracking “variants of indifference?”
By which I mean variants that do the expected thing where mutations increase transmissibility but decrease virulence?
The logic of natural selection would tell us those should be the much more common kinds of variants as they should increase the changes of newer generations of virus surviving to reproduce.
It’s strange to me that all of the variants discussed have both increased transmissibility and virulence. It seems anti-Darwinian.
If there are thousands of VOIs (variants of indifference), which you might predict for every VOC, could that not have an effect on the overall statistics? More people get less virulent VOIs and some immunity?
Although it is widely held by biologists that there is a tradeoff between infectiousness and virulence, people (eg, Paul Ewald) who actually study the evolution of virulence say the opposite, both in theory and data. In the case of sars2, it is overdetermined: death is due to immune overreaction, after the window of selection is over.
Does he have anything to say about the case of sars-Cov-2 specifically?
On one hand, yes it seems like there’s something like antagonistic pleiotropy here where most of the transmission is done before the “acute phase” (the time when your o2 sat drops and you go to the ER, there’s probably a better term for that I’m just not sure what it is).
But we’re also applying non-trivial selection pressure via lockdowns and other precautions, and if sars-Cov-2 would stop killing people and just give them a runny nose we would stop and it could reproduce more. I’m just not certain why that isn’t have more of an effect.
That’s a group selection argument.
Not trying to be antagonistic, but how so? It applies individually to each virion that would have a mutation that decreases its virulence.