[someotherperson]

Since this will continue to be misunderstood, it's important to emphasise that the article explicitly mentions that there is

1. No evidence to support the idea of strains that have any impact on infection

2. No evidence to support the idea that the strains will resist the vaccines or weaken vaccine efficacy.

This is not a "strain" in the sense of the flu, COVID-19 hasn't fundamentally changed in any meaningful way that lets us do anything other than track the pandemic's spread.

[VLM]

The problem with "any" is its usually wrong. Here's an "old" paper from July:

Toyoshima, Y., Nemoto, K., Matsumoto, S. et al. SARS-CoV-2 genomic variations associated with mortality rate of COVID-19. J Hum Genet 65, 1075–1082 (2020). https://doi.org/10.1038/s10038-020-0808-9

The measured variation between the now extinct L strain and the new current G strain is the G strain was about 2% higher correlation between strain and fatality rate. The actual fatality rate was not 2% higher which would be huge, but the % of L in a population vs population fatality rate correlated 2% higher based on euro country data in the spring.

Certainly there's only two real impacts on fatality rate right now, both incredibly politically incorrect to discuss, there's an enormous staggering stunning huge disparity in fatality rate by age, and a merely giant disparity in fatality rate by comorbidity rate. The medical science seems clear, but the political impact makes it impossible to discuss quarantine policies that would minimize total death rates. Hundreds of thousands of lives could be saved by locking up everyone over 60 and everyone over 300 pounds and a couple other pre-existing conditions, but AARP is one of the strongest PACs out there and even if it saves her life, grandma will vote out anyone who "locks her up for a year for her own good".

Personally I'm old enough that I'm working very hard to max out my cardio health for when I inevitably get it.

[rossdavidh]

Well, that's _mostly_ true, but the very fact that one virus variant displaces another over the course of a month or two, while by no means definitive proof of anything, is at the very least suggestive that for one reason or another it is better able to spread.

It _could_ be a neutral mutation that just spread due to a "founder affect" or something, but it would not be in any way surprising if a virus which is brand new in humans, evolved in the direction of adapting better to that new environment. What spreads better in bats, may not be the same as what spreads better in humans, and there is no particular reason to expect that this virus wouldn't be mutating in the direction that allows it to adapt to its new host.

Now, that could even be a good thing, if it was adapting in the direction of not triggering the host's immune system as strongly, since it is largely an immune system overreaction that kills the host. But, while by no means definitive, I don't think we can say that there is _no_ evidence to support the idea that strains have any impact on infection. the very fact that the initial strain has been largely displaced by others, suggests at least the possibility that it has.

[riccia]

Not questioning anything you wrote, but it would be interesting to know the strains of virus in people who acquired COVID in the mRNA vaccine trials. I imagine this is in the trial data but haven't seen it.

[CyberDildonics]

How many people actually acquired COVID in the mRNA vaccine trials?

[lvs]

In the BioNTech vaccine Phase 2/3, it was 50 any time after the first dose, but 11 after the second dose.

[CyberDildonics]

Those were people who caught covid or people that had antibodies?

[lvs]

Patients who received one or two doses of the vaccine who later tested positive for covid.