| > The point of the argument here, from my point of view, is this. In the one to three months between full vaccination of vulnerable individuals and drastically reduced R due to general vaccination, Not a given. It's very likely, but we don't know how effective the vaccines will be in preventing transmission. Certainly there is past precedent for the opposite. Also, there's likely to be pockets of population with poor vaccine penetration, so even if it confers sterilizing protection, we're likely to see endemic spread in these subpopulations continually challenging the vaccinated population. > is a variant of the virus going to appear that will be able to effectively infect vaccinated people and spread enough for the pandemic to continue? We see a hepatitis B vaccine escape variant every year or two, despite a much lower community disease burden. I don't think anyone can know how likely this is. > All of this would have to happen in a subset of the population that has a 20x lower chance of being infected and even when that happens, It's not very likely that the population has a 20x lower chance of being infected; the vaccine almost certainly does more to prevent symptomatic illness than any infection. They've shown a 20x lower chance of symptomatic illness. You're also leaving out the critical window before the first dose where protection (against symptomatic illness) slowly climbs over weeks to 70-80%. > It would also have to compete effectively against other variants in the non-vaccinated population while it is doing so Already the currently circulating variants are not equally neutralized by the vaccine. There's going to be immediate pressure making the variants that are least impeded more prevalent. > unless you believe that these extensive mutations will happen in one, vaccinated, patient, which is pretty much impossible. Again, the most likely scenario for the emergence for the UK variant is prolonged infection in one person with a low immune response. People like this are well represented in the groups we're immunizing first, too. These things aren't mutually exclusive, though: you start off by favoring the current variants that the vaccine is least effective against. Then, you have ongoing evolution in vaccinated individuals with lower responses. Then the favored variants become endemic, circulating mostly in subpopulations with lower vaccine coverage and occasionally finding vaccinated people who are more susceptible. How quickly it all happens depends upon total disease burden. I agree we will probably not get a worst-case escape variant in the first few months of the vaccination campaign, but I think we'll probably see some adaptation towards escape and lowered efficacy. Indeed, you don't even need mutation for that: just preferential selection for existing variants with lower vaccine efficacy. No one's done the assays on the UK variant yet, but I will not be surprised if the current vaccines are somewhat less effective against it. If the disease remains endemic with relatively high levels of circulation, variants that escape the current vaccines will be all but certain in the long term. |
Hepatitis B is a disease that lasts much, much longer than COVID-19, which exponentially increases the likelihood of such an event. Moreso, Hepatitis B immunity from vaccines is often very weak due to a lot of people not getting booster shots in adulthood.
>It's not very likely that the population has a 20x lower chance of being infected; the vaccine almost certainly does more to prevent symptomatic illness than any infection. They've shown a 20x lower chance of symptomatic illness. You're also leaving out the critical window before the first dose where protection (against symptomatic illness) slowly climbs over weeks to 70-80%.
Vaccines have been trialled using not symptomatic illness, but actually PCR tests for immunity, and found over 90% immunity with symptoms||viralRNA as a standard. So no, it's actually around 10-20x less likely to have infection, too. For things like severe ilness, it's more like 99-100%.
>It's not very likely that the population has a 20x lower chance of being infected; the vaccine almost certainly does more to prevent symptomatic illness than any infection. They've shown a 20x lower chance of symptomatic illness. You're also leaving out the critical window before the first dose where protection (against symptomatic illness) slowly climbs over weeks to 70-80%.
During this window if the individual is vaccinated before antibodies show up there is very little pressure to evolve resistance against them.
>Again, the most likely scenario for the emergence for the UK variant is prolonged infection in one person with a low immune response. People like this are well represented in the groups we're immunizing first, too.
Given the fact that we have seen zero severe illness in even very old people with many vaccines, this is even less likely than for a non-vaccinated but immunocompromised person, for which this scale of mutation didn't even happen yet, 1 year in. And by the way, the hypothesis - which is as of yet unconfirmed and whose certainty became lower after similar mutations were found in South Africa - is that this process happened in an unvaccinated immunocompromised individual during a month+ infection period. If the same individual was vaccinated, this would have been impossible, and we haven't seen this kind of illness in any vaccinated individuals.
>These things aren't mutually exclusive, though: you start off by favoring the current variants that the vaccine is least effective against. Then, you have ongoing evolution in vaccinated individuals with lower responses. Then the favored variants become endemic, circulating mostly in subpopulations with lower vaccine coverage and occasionally finding vaccinated people who are more susceptible.
Even for those, the vaccine is still incredibly efficacious. The differences IIRC are barely statistically significant. If you have a source for more significant variations I'd love to see it.
Crucially though, in the scenario you are suggesting where the virus is spreading in non-vaccinated populations, that the actual strain to acquire enough changes to become effective against vaccinated individuals absolutely needs to outcompete other strains, which isn't likely. This is because even if the virus were to infect one of the few vaccinated but less protected individuals, which would in this case probably be under 1% of infections, those mutations need not be a hindrance in the 99% of infections which won't be of less protected individuals that have more than benign infections in populations with low vaccination rates.
It's possible that this happens, eventually - think years. Not in the 1-3 months period we're talking about. The result is that it doesn't make sense to vaccinate 20-40 year olds in priority or to sell the vaccine on the free market, at all.