The IFR seems to be about 1% now that we a have a lot of data, and a bit higher in the US. But that could change or are you asserting it won't? And are you completely unconcerned about new variants? We'll have to disagree on that. The Delta variant has saturated ICUs again, no problemo I gather?
And you're misrepresenting the paper. It doesn't claim 35% fatality, it cites the 35% fatality of MERS, a distantly related coronavirus and the 10% fatality of the original SARS pandemic, a closer related virus (1), both mostly settled science, as potential upper bounds of what variants could emerge if we don't get this under control.
Viruses evolve to do one thing: make more virus particles. If there is a gain of function that increases the fatality rate then so be it. Usually they become less deadly because that makes them spread more effectively but there are exceptions. It's comforting to assert that it's impossible for a virus to evolve to become more deadly but it's also false.
> But that could change or are you asserting it won't
How can you interpret what I wrote to say that a new virus or variant certainly won't cause a higher fatality rate? Anything can happen at any time. For all we know, a new virus could become prevalent. Typically though, we base public policy based on things that have already happened and the likelihood of future things.
There is little reason to believe COVID will evolve into something more deadly. In general viruses rarely make this evolutionary step. Pathogens do not gain reproductive advantage by killing their host. This is why zoonotic pathogens are so dangerous ... when such a pathogen crosses over, they can go from causing no damage to their original host (bats) to becoming very deadly in the context of a human body. Indeed, if history is any guide, endemic human viruses eventually evolve to be mild infections or beneficial (there are theories that placental development is due to the presence and integration of ancient viruses in mammalian DNA).
Given that, unlike the flu which has natural reservoirs in birds and crosses over very frequently to humans, COVID does not seem to be bouncing between animal hosts, it is highly unlikely based on every understanding I have of pathogenic evolution that the virus will become more deadly. Indeed, delta variant, while more infectious (as to be expected) is not as deadly.
> . It doesn't claim 35% fatality, it cites the 35% fatality of MERS, a distantly related coronavirus
Except, MERS and SARS-Cov1 are zoonotic viruses, whereas the COVID variants are human evolved and thus unlikely to become more pathogenic. Zoonotic viruses evolve to be less deadly in their hosts. The zoonotic crossover is a chance event and given the viruses were evolved to not kill bats, they had not been exposed to any selective pressure to not kill humans. Now they are exposed to that pressure so we will see the fruits of that selection.
Also, as you point out, MERS is only distantly related. If this pandemic were MERS with a higher infection rate, then it would have been more concerning to begin with, but of course then it would also have evolved faster to be less pathogenic because the selection pressure would be stronger. But it's not. Even the earliest estimates (again, with assuredly bad data) were a fatality rate of 7-8%. They've gone drastically down, by orders of magnitude, and the new variants will continue to drop that.
It is good new variants are being created. The higher infection rate + lower death rate will lead to quicker herd immunity against a broader spectra of Sars-COV2 family viruses.
So you assert viruses cannot evolve to be deadlier but at the same time insist they always evolve to become less deadly.
But the only evolutionary imperative is more virus particles. If becoming less deadly is the best path, the virus becomes less deadly. But if increased fatality comes along with making more virus particles, it will get deadlier. But don't take it from me:
"But there’s no obvious evolutionary advantage for SARS-CoV-2 to reduce its virulence, because it pays little price for occasionally killing people: It spreads readily from infected people who are not yet feeling sick, and even from those who may never show symptoms of illness." - https://www.smithsonianmag.com/science-nature/how-viruses-ev...
>COVID does not seem to be bouncing between animal hosts
35% is the fatality rate of MERS, a related CoronaVirus, and you have presented zero evidence to prove it's impossible SARS-CoV-2 mutate up to that rate. You sound like you're trying to cover up peer-reviewed data suggesting we take this into account. You have also presented no evidence that with increased transmissibility we won't see increased fatality. Put up or shut up.
Viruses don't 'mutate' up to a death rate. They mutate to a low death rate in one host, then sometimes cross, and happen to cause a higher death rate in the new species.
Can Sars cov2 cross to another animal, mutate, and come back to humans with a higher death rate? Certainly, but that's not what we're talking about with these variants.
So you are asserting it is impossible for a virus to increase its fatality rate through mutation within the same species? That there has to be a zoonotic transfer for this to be possible? Where's your evidence? Because this must mean that contrary to the prevailing belief across the scientific community that Spanish Flu did exactly that (1), there must have been 2 Zoonotic events transfer events between the first and second wave.
You're looking at a Nobel Prize here if you're right, take your best shot sport!
> It also says that in addition to being more contagious, the delta variant likely increases the risk of severe disease and hospitalization, compared with the original strain.
Hold on, hospitalization and severe disease and death are completely different things. This is a disingenuous use of this article.
I mean, mono is severe (tired for months potentially), but not deadly. A burst appendix requires hospitalization and is a severe medical emergency, but is not deadly in the developed world. We can go on...
"hospitalization and severe disease and death are completely different things."
So you're claiming hospitalization, severe illness, and death are not correlated at all w/r to prior of COVID-19 diagnosis? How does that work? Do you have the numbers to back this up? I'd love to see them.
And you're misrepresenting the paper. It doesn't claim 35% fatality, it cites the 35% fatality of MERS, a distantly related coronavirus and the 10% fatality of the original SARS pandemic, a closer related virus (1), both mostly settled science, as potential upper bounds of what variants could emerge if we don't get this under control.
Viruses evolve to do one thing: make more virus particles. If there is a gain of function that increases the fatality rate then so be it. Usually they become less deadly because that makes them spread more effectively but there are exceptions. It's comforting to assert that it's impossible for a virus to evolve to become more deadly but it's also false.
1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7718587/