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Originally Posted by opendoor
I will say, blankall's original point (at least what I think he was getting at) is a fair one. At this point, unvaccinated people aren't going to be the population that drives mutations, because most of them have had COVID already. So the idea of the unvaccinated being variant factories is more of a relic of pre-Omicron when they were basically the only ones getting infected in any real numbers.
And yes, it's true that widespread immunity will put evolutionary pressure on mutations to get past that; that's just the reality. But ultimately, high levels of immunity will tend to depress the the rate of troublesome variants, potentially significantly. In the 7 months that Omicron has been dominant, we've seen probably 10-20x as many infections as we saw in the period that resulted in Alpha, Beta, Delta, and Gamma coming about, but so far there hasn't been a significant level of change in either severity or immune escape. And that's with a relatively large portion of the world's population still being immunologically naive before Omicron took over (about 40% of the world's population isn't vaccinated).
And beyond that, there's no real option in the matter like there is with antibiotics. We can be stricter with antibiotic use in order to delay antibiotic resistance and generally have similar health outcomes (i.e. by only using antibiotics when necessary and by following the full course). There's no other path we can take with a circulating respiratory virus. We're all going to be repeatedly exposed to it and will generate immunity one way or another (whether that's through infection, vaccination, or a combination of both).
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For the record, I was in no way arguing against vaccination. It's an excellent form of immunity and has been proven to decrease the severity of infections. Once again, the acquired immune response from vaccination has been shown to be far less deadly than the purely innate immune response you see in those with no pre-existing immunity.
This is a great article that talks about how the roles of the various parts of the immune system:
https://www.nature.com/articles/s41418-022-01015-x
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Pro-inflammatory macrophages are the major immune cell type that expresses high levels of ACE2 [38]. Upon SARS-CoV-2 infection, these macrophages release inflammatory cytokines and chemokines including C-C motif chemokine ligand 7 (CCL7), CCL8 and CCL13 to recruit and activate T cells. In turn, T cells produce IFN-γ and other cytokines to further activate macrophages [39]. This positive feedback loop drives the elevation and continuation of the pathological inflammation. Epidemiological data show that older adults and people with underlying health conditions exhibited a dramatically high rate of severe disease and mortality [17]. Along with aging, there is a tendency of increasing inflammatory macrophages [40]. This not only explains why chronic inflammatory disease occurrence is more prevalent but also provides a possibility accounting for the high incidence of severe COVID-19 cases in older people. Along with this scenario, it is reasonable to comprehend why SARS-CoV-2 infection in those with underlying medical conditions also exhibited a higher prevalence in severe disease and mortality [12].
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Basically you want ot avoid a high inflammatory response in favor of a targeted immune response.
Doesn't change the fact that the next strain that needs to spread, will have to be one that mutates to avoid existing immunity, and that is only likely to occur in someone with existing immunity.