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Comment by berkut | Hacker News Reader

There seems to be some evidence that having a longer duration between the first and second doses provides better long-term protection, i.e. gaps of 7+ weeks, compared to the 3+ weeks the US and Israel have generally done.

NZ is currently thinking about increasing the gap to > 6 weeks because of this.

I wonder how much that would affect things.

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I heard that as well. My feeling is that with all the treatments we are deploying against the virus, one thing we are doing is creating a selective pressure, forcing it to evolve to promote more resistant and transmissible variants. Whether those transmissible variants also contain higher mortality might be a crapshoot game of chance, but I don't hear this sort of idea spouted a lot and I think it's worth considering. It might be similar to the way that antibiotics have helped select for 'treatment-resistant' 'superbugs'.

Increased transmission is worse than increased fatality rate, counterintuitively, as it's the same percentage deaths of a much much higher number infected - resulting in higher numbers of absolute deaths than if the CFR increased without an increase of transmissibility.

Ah, that's a great and simple and direct explanation of that. Thanks, I'm gonna try to remember that.

Vaccines are very different from antibiotics. Antibiotics are single molecules that bind a very specific target. A single mutation of a single protein can render an antibiotic useless. Vaccines induce the immune system to generate a repertoire of antibodies, each of which binds in a different way and each of which is then selected and "evolved" (hypermutation) for increased efficacy. And each individual person creates a different starting and ending repertoire of antibodies. A single mutation, or even a large group of mutations, does not so easily side step all this diversity of antibody types/binding modes. Moreover, we have evidence that the idea that vaccines increase the likelihood of variants is just wrong. We do not see that effect for mumps, polio, smallpox, or any other virus. Moreover, delta appears to have arisen in India, which at the time had vaccination rates very close to zero. Again, providing strong evidence that vaccines are not applying selective pressure for more virulent strains.

That's interesting. it's a good argument. Maybe vaccines are the answer. But I don't think we can rule it out and say it's 'just wrong' tho right?

The delta and lambda variants emerged, and they were both more transmissible, and more vaccine resistant, is that right? I mean, why do you need to evolve vaccine resistance and transmissibility at the same time? Seems weird, and given the 'shotgun' quality of antibodies across individual and population, particularly so.

Which lets me feel that we are applying some selective pressure with vaccines. Compared to the other virus mentioned, what's different is the scale and rate of vaccine roll out here is unprecedentedly greater. Maybe in the previous cases our immune system had already evolved stronger defenses by the time the vaccines were given, 'patching more holes in the dam' so to speak.

> Moreover, delta appears to have arisen in India, which at the time had vaccination rates very close to zero.

For the sake of clarity, the first viral genome of B.1.617 (eventually named Delta) was identified by India's variant tracking program on October 5, 2020, long before any vaccines were approved. India's case load was also quite low at this point, and the initial lockdown was being slowly rolled back.

The bottom line is, it's that after second vaccination amount of antibodies start to decline and at some point of time efficiency of vaccination going down with it. The "better" long term protection by longer gap between doses probably just buys extra couple of months or so of good efficiency at cost of lowered between two shots

Yet you will have a period of time where the person that waits for second dose would have an increased risk compared to normally schedule one.

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