Why are we seeing new variants emerge in several locations independently in a short time window? Is it that people are looking more closely now? Or does virus evolution have a kind of “molecular clock” based on law of large numbers? Or is the “clock” here mostly the time it takes a more infectious variant to become dominant enough to get noticed, and the count started whenever plasma therapy was used or whatever else happened with immunocompromised patients? Should we expect new more infectious variants to spring up all over the world in high-prevalence locations in the next couple of weeks anyway, regardless of whether the UK/SA/Nigeria variants made it there via plane?
AFAICT the reason immunocompromised patients are important is they can stay infected for several months. I read a paper recently where such a patient held on for about 5 months, and by my count, samples averaged 3 mutations per month (although I’m sure there’s a better way to adjust the numbers than what I did). So there’s time to infect enough IC’d patients, plus n months to evolve in them. If antibodies are a necessary ingredient that would delay these steps more. Then there’s time for the highly fit strain to outcompete other strains, which is proportional to 1ln(Rfit/Rother). And finally, time to establish the strain is growing and time to check for evidence of causality.
IIRC the UK strain became a major issue later, but the UK has nearly the best genome surveillance which is why the announcements happened so close to each other. Fuzzy on the timelines, but I think SA announced theirs later. Maybe SA decided to call the press due to the UK announcement instead of waiting for better proof? And/or sped up the search for evidence.
Regardless, assuming both are legit, the close announcement times seem to be mostly coincidence. But I think we should expect other strains with large jumps in R to start being an issue soon, even if most won’t be recognized as quickly.
I notice I’m confused- SA’s variant, if legitimately due to a huge jump in R, doesn’t have huge numbers of mutations.
If the UK variant had a 45% jump in R, and SA’s has a 20%, and >20% is much more commonly due to IC’d patients, then it seems reasonable that the super-fit, highly mutated strains show up alongside the more mundanely fit, moderately mutated ones. The super-fit’s take longer to bake but they take off faster. But then again I’m trying to make a theory to explain 2 data points that I’m not 100% are both correct, so as much as this feels correct it probably isn’t.
So the emerging wisdom is that the SA variant is less contagious, or are you just using 20% as an example? The fact that SA is currently at the height of summer, and that they went from “things largely under control” to “more hospitalizations and deaths than the 1st wave in their winter” in a short amount of time, makes me suspect that the SA variant is at least as contagious as the UK variant. (I’m largely ignoring politicians bickering at each other over this, and of course if there’s already been research on this question then I’ll immediately quit speculating!)
Oops, missed this. I don’t check LW messages much.
20% was not an exact value. At the time I wasn’t aware of any estimates. Since then I’ve heard that the standard curve fit returns a ~50% growth per 6.5 days, some or all of which may be due to immune escape.)
I had a couple assumptions that made me think the SA strain was less contagious in expectation:
High contagiousness is more likely when high mutation numbers were seen, and correspondingly emergence would tend to be later. The SA variant gained local dominance earlier than the UK.
There was (and is) much less data on the SA variant. Due to the high variation in number of infectees per sick person, my prior is that on average, a variant that seems to be gaining ground is not as infectious as a curve fit implies, because luck could be a big factor and is more common than extreme fitness.
Why are we seeing new variants emerge in several locations independently in a short time window? Is it that people are looking more closely now? Or does virus evolution have a kind of “molecular clock” based on law of large numbers? Or is the “clock” here mostly the time it takes a more infectious variant to become dominant enough to get noticed, and the count started whenever plasma therapy was used or whatever else happened with immunocompromised patients? Should we expect new more infectious variants to spring up all over the world in high-prevalence locations in the next couple of weeks anyway, regardless of whether the UK/SA/Nigeria variants made it there via plane?
AFAICT the reason immunocompromised patients are important is they can stay infected for several months. I read a paper recently where such a patient held on for about 5 months, and by my count, samples averaged 3 mutations per month (although I’m sure there’s a better way to adjust the numbers than what I did). So there’s time to infect enough IC’d patients, plus n months to evolve in them. If antibodies are a necessary ingredient that would delay these steps more. Then there’s time for the highly fit strain to outcompete other strains, which is proportional to 1ln(Rfit/Rother). And finally, time to establish the strain is growing and time to check for evidence of causality.
IIRC the UK strain became a major issue later, but the UK has nearly the best genome surveillance which is why the announcements happened so close to each other. Fuzzy on the timelines, but I think SA announced theirs later. Maybe SA decided to call the press due to the UK announcement instead of waiting for better proof? And/or sped up the search for evidence.
Regardless, assuming both are legit, the close announcement times seem to be mostly coincidence. But I think we should expect other strains with large jumps in R to start being an issue soon, even if most won’t be recognized as quickly.
I notice I’m confused- SA’s variant, if legitimately due to a huge jump in R, doesn’t have huge numbers of mutations.
If the UK variant had a 45% jump in R, and SA’s has a 20%, and >20% is much more commonly due to IC’d patients, then it seems reasonable that the super-fit, highly mutated strains show up alongside the more mundanely fit, moderately mutated ones. The super-fit’s take longer to bake but they take off faster. But then again I’m trying to make a theory to explain 2 data points that I’m not 100% are both correct, so as much as this feels correct it probably isn’t.
So the emerging wisdom is that the SA variant is less contagious, or are you just using 20% as an example? The fact that SA is currently at the height of summer, and that they went from “things largely under control” to “more hospitalizations and deaths than the 1st wave in their winter” in a short amount of time, makes me suspect that the SA variant is at least as contagious as the UK variant. (I’m largely ignoring politicians bickering at each other over this, and of course if there’s already been research on this question then I’ll immediately quit speculating!)
Oops, missed this. I don’t check LW messages much.
20% was not an exact value. At the time I wasn’t aware of any estimates. Since then I’ve heard that the standard curve fit returns a ~50% growth per 6.5 days, some or all of which may be due to immune escape.)
I had a couple assumptions that made me think the SA strain was less contagious in expectation:
High contagiousness is more likely when high mutation numbers were seen, and correspondingly emergence would tend to be later. The SA variant gained local dominance earlier than the UK.
There was (and is) much less data on the SA variant. Due to the high variation in number of infectees per sick person, my prior is that on average, a variant that seems to be gaining ground is not as infectious as a curve fit implies, because luck could be a big factor and is more common than extreme fitness.
Conditional on a 4th wave in the US happening in 2021, I wonder if it’s >20% likely that it’s going to be due to a variant that evolved on US soil.