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Comment by colechristensen | Hacker News Reader

There are evolutionary pressures on viruses that tend to weaken them over time. You get variants competing with each other and the more silent ones get advantages over the ones with worse outcomes.

It isn’t clear exactly what is going to happen, but as more people get vaccinated and natural immunity and the variants continue to evolve the situation might change a lot or become unnoticeable.

I would love to see an epidemic expert comment on the long term evolutionary effects of different mitigation strategies which might differ in preferences than short term trying to reduce number of infections.

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> There are evolutionary pressures on viruses that tend to weaken them over time.

Those evolutionary pressures relate to transmissibility. Basically, a virus that kills its host before it can spread doesn't spread very far at all.

SARS-CoV-2's defining feature of asymptomatic spread decouples this and so far hasn't led to weakening – indeed, Delta is both substantially more transmissible and more likely to cause severe disease and death.

Right, and because of severe disease and death health authorities introduced more stringent rules to reduce transmission. Evolutionary this should eventually pressure the virus in to becoming less severe (assuming public health policy continues to be focused on preventing severe disease and death).

This assumes a uniform global response. Not even the US can get their pandemic under control. There are so many breeding grounds across the world where Covid is completely free to mutate that it doesn't matter if a handful of countries have it figured out. You also have an increasing pushback against measures even in European countries with high vaccination rates. If a high impact variant emerges, it's going to become harder and harder on a political (and even economic) level to contain it.

> Not even the US can get their pandemic under control.

That's because the vaccines don't effectively stop the spread of SARS2. This is one of the great lies still being shoveled on the public - despite the facts that prove otherwise.

See: Britain has a lot more cases per capita than the US, despite their high vaccination rates and more aggressive lock-down & restrictive measures taken.

Or see: the New England states with high vaccination rates and a recent record surge in cases.

Or see: Israel's recent epic case surge despite their very high vaccination rate.

The vaccines dramatically reduce mortality and that's the primary reason most people should get the jab. There's zero evidence so far that we can actually stop SARS2 via vaccine. It doesn't make sense to be forced to live in bomb shelters forever as eg Australia is doing, that's idiotic and tyrannical. What matters isn't the case counts, it's the number of deaths that matter and Britain's high vaccination rate is doing its job there for example.

> Or see: the New England states with high vaccination rates and a recent record surge in cases.

As a resident of New England, I've been expecting a fall surge for a while. In the north, we're all shutting windows and turning on our furnaces at night, which means much worse ventilation. The afternoons are still warm enough to socialize outside, but that will start to change in November. Followed by holiday travel. And we still have towns with low vaccination rates.

Our absolute numbers are still fairly low in many places, and we don't have people lined up in the corridors of the local hospitals.

> What matters isn't the case counts, it's the number of deaths that matter

I actually think that severe illness counts are important, too. I'll make some sacrifices to avoid hospitalization or merely being incapacitated for a couple weeks.

The need to achieve immune escape can also pressure the virus to evolve antigenically which can promote transmissibility through escape, while impairing ACE2 binding or endocytosis compared to currently circulating variants.

So if the ancestral strain + variants all cannot spread epidemically any more due to the build up of immunity in the population, then a strain which achieves immune escape and an R0 of > 1.0 would be favored even though the virus might be much less "fit" and less virulent in a totally naive population.

Clearly though the major adaptation is going to be on the human side with most of the population eventually acquiring T-cells, which will greatly decrease the virulence going forwards.

> while impairing ACE2 binding

It appears that COVID-19 can also enter cells (these would be immune cells that came to 'help') via so called Fc-pathway.

Therefore allow the virus to multiply even more

"... In addition to viral entry via ACE2, antibodies against coronavirus spike proteins (anti-spike-S-IgG) can induce antibody-dependent enhancement (ADE) of viral entry via type II Fcγ receptors. ..." [1]

[1] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7406916/

That really has nothing to do with what I wrote, other than for you to write about ADE, which is not a practical issue for anyone to worry about with SARS-CoV-2:

https://www.science.org/content/blog-post/new-antibody-depen...

I can't flag you, but someone else really should since your followup is completely disingenuous.

sorry, but your assessment of what is genuine vs disingenuous, is very disingenuous in itself.

Perhaps, it is time to relinquish the presumptions of moral superiority -- and just discuss technical details without the drama ...

I am saying that you wrote does not cover full spectrum of how the virus replicates, therefore your comment does illuminate the complexity that's present in interaction with our immune system. Which includes, according to the NIH paper I referenced, antibody-dependent-enhancement (ADE).

If you saw any form of antibody-dependent enhancement, signals would be far spread now, considering how much viral spread is occurring...

> However, using monkey and mouse models of SARS-CoV-2 infection, none of the in vitro infection-enhancing Abs enhanced SARS-CoV-2 virus replication or infectious virus in the lung in vivo. Three of 46 monkeys had lung pathology or bronchoalveolar lavage (BAL) cytokine levels greater than controls. However, repeat studies with dose ranges of in vitro enhancing Abs did not increase lung pathology. Thus, in vitro infection-enhancing RBD and NTD Abs controlled virus in vivo and was rarely associated with enhanced lung pathology. [1]

1: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8232969/

That isn't relevant to the discussion at hand in any way shape or form.

You're interjecting it because you want to talk about it because you're an antivaxxer.

It has no relevance outside of some narrow understanding of what happens during severe COVID itself and the mechanism behind why some people get very sick and most people do not.

And you're practicing sealioning acting like you're just innoccently interjecting.

Which is what makes what happened with Marek's disease so interesting.

Presymptomatic might be a better term than asymptomatic, as the evidence for asymptomatic spread is weak and weakening. One example[1]:

> Research early in the pandemic suggested that the rate of asymptomatic infections could be as high as 81%. But a meta-analysis published last month, which included 13 studies involving 21,708 people, calculated the rate of asymptomatic presentation to be 17%. The analysis defined asymptomatic people as those who showed none of the key COVID-19 symptoms during the entire follow-up period, and the authors included only studies that followed participants for at least seven days.

There are many more I've read where the authors have tried to quantify asymptomatic spread and been found wanting (studies on children are particularly enlightening). I wouldn't be surprised if the final figure ends up being very close to, if not, zero, though we're still in the clutches of the initial panic so I suspect those findings to take time due more to social resistance than the frictions involved in actual science.

[1] https://www.nature.com/articles/d41586-020-03141-3?error=coo...

Note that I said "asymptomatic spread", not "asymptomatic infection" – i.e. a host spreading SARS-CoV-2 without experiencing or showing symptoms from the active infection. Whether the host goes on to experience symptoms from said infection at some point in the future isn't what I was referring to.

Right, and that changes nothing about my response as that's what I was responding to, there is still weak and weakening evidence for transmission by those with asymptomatic infection.

For example[1]:

> We determined secondary attack rates (SAR) among close contacts of 59 asymptomatic and symptomatic coronavirus disease case-patients by presymptomatic and symptomatic exposure. We observed no transmission from asymptomatic case-patients and highest SAR through presymptomatic exposure.

[1] https://wwwnc.cdc.gov/eid/article/27/4/20-4576_article

You seem to be misunderstanding me here. When I say "asymptomatic transmission," I am referring to whether or not a person is displaying/experiencing symptoms at the time of transmission.

"Presymptomatic transmission" is asymptomatic transmission. Whether the infection itself becomes symptomatic later (which, as you've referenced, the research strongly suggests will happen) is of no relevance to the discussion.

You're just using a definition that none of the papers I've read use when trying to make a useful distinction. Asymptomatic as a term is distinct from presymptomatic the moment presymptomatic is used, or there would need to be another word for those who remain asymptomatic, and that word is, unsurprisingly, asymptomatic.

> Whether the infection itself becomes symptomatic later (which, as you've referenced, the research strongly suggests will happen) is of no relevance to the discussion.

What's actually irrelevant is talking about asymptomatic infections - defined as those which do not become symptomatic - as if they do become symptomatic. Again, I'm yet to find a paper that does this. Whether or not an infection is more likely to become symptomatic or not is not relevant here, nor did I make reference to any such likelihood, because it's not relevant.

I can't tell if you're quibbling because you don't want to accept a minor correction or because you haven't bothered to read any of the literature.

> tend to weaken them over time

Perhaps you could furnish us with some examples of such viruses? Every virus I can think of certainly hasn't weakened over time.

The 1918 “Spanish” influenza pandemic that killed 1-5% of the human population still has descendants in circulation both direct and through horizontal gene transfers. Basically all influenza A infections contain at least a piece descended from 1918.

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