jsnell
1890
It is reasonable. Last December, they’d had just shy of 1M confirmed cases. At the same time, serological surveys were estimating 25% = 15M of the population having been infected.
Either a lot of cases have been missed, or the serological surveys were grossly wrong. But you’d expect the number of false positives to be about 1% on those tests, not 20%.
Yes, that’s clear. Thanks for taking the time to explain the basis.
All of this is why I’ve been taking any information posted out of SA with a huge grain of salt.
Are these the lessons that a layperson (i.e., my wife and family) should glean from the currently-available Omicron data?
- Omicron looks to be far more transmissable than Delta.
- Omicron looks to be far less dangerous than Delta.
- Given the above, it’s likely that case counts are going to explode in the next few months, but hospitals won’t be as overwhelmed as they were with Delta.
- It’s still very early, so this can all change once we get more data.
I still think we’re at too early to say too much conclusively. One reason for the “mild” suppositions I’ve seen is that vaccination/previous infection creates milder disease, because B Cells adapt, and T Cells are a thing that works.
But if Omicron is more transmissible by the rate it seems to be, that means that it has the possibility to cast a fairly wide net on infections. So even with a lot more milder cases/asymptomatic cases, you’re maybe looking at a small percentage of a very large number, which in raw numbers still creates the possibility to overrun healthcare providers.
Truth of it is: we still just don’t know yet.
KevinC
1896
My approach has been the more confident a person is proclaiming to know the effects of Omicron, the more skeptical I should be of what that person is saying.
At this early stage, anyway. That will obviously change with more data.
Yeah, I think that’s a concern: even if % of patients needing hospitalization is much lower, the increased transmission could outweigh that.
Qmanol
1898
Just from reading around, here’s my general impression of what we kno at this moment in time:
Omicron seems to be absolutely more contagious, probably by quite a significant margin.
It’s probable that at least some of that is due to antibody evasion, which would significantly reduce the effectiveness of immunity in preventing infection. Immune escape alone does not appear to be enough to explain the greater contagion at this point.
Immunity against severe disease is probably also impacted, but less so due to T and B-cell immunity which come into play after infection. How much less is still in question.
Omicron is causing milder disease, but at present we don’t have enough data to tell if that’s due to it being less virulent or due to existing vaccine/infection based immunity. It is still possibly just as virulent as Delta but seems “milder” because it’s more able to infect the vaccinated who then have a milder illness.
JonRowe
1899
Historically, this is how a lot of flu/viral strains go, as transmissibility goes up, illness severity goes down. The selection pressure of making people so ill they die or stay at home hurts the transmissibility part, so variants that tend to have high transmissibility win out, because they don’t make people as ill.
Hopefully that is what we are seeing here, but not enough data at this time.
A virus is a living organism, driven by the need to reproduce. Wouldn’t its “final form” be one that’s super contagious but doesn’t kill its host? Then it can spread and thrive, as biology demands.
Or. what Jon said.
Don’t assume evolution is some perfect mechanism, things just need to be good enough. Blah blah law of large numbers but any individual species can be the exception.
Is it not a form of survivorship bias? No species-ending plagues are possible because none have ever happened.
As long as it can reproduce and spread to another host before the host dies, it doesn’t matter much if the host dies.
jsnell
1904
As a counter-example rabies has been around forever, and is 100% fatal to humans without modern medical care.
The textbook example for the kind of thing you’re talking of is the myxoma virus that was introduced into Australia to kill the rabbits. At first it had a mortality rate of 99.6%. But then over the next decade various milder versions appeared, leveling out at around 50%. That’s proof of the virus evolving to be less virulent, as predicted! Except that one decade later, the 50% lethal version had died out and the dominant strain killed 75-90% of the infected rabbits. Why? Because the virus spread over lesions, and the more lethal straints caused longer lived lesions than the “mild” ones, allowing for more infections to happen.
Covid doesn’t benefit a lot from becoming less lethal. By the time somebody dies, their usefulness to the virus is over. Heck, it doesn’t even really benefit from becoming less severe otherwise, since it appears to be so effective at spreading pre-symptomatic and has no need to be stealthy.
Aceris
1905
However, a less lethal variant might be a pre-requisite for the kind of mutations that occured here, where COVID reproduced across many many generations in an immunocompromised host (we think maybe).
jsnell
1906
The “doubling every two days” rates of Omicron growth vs. Delta in the European countries with proper monitoring continue:
What is expected, as far as I understand it, is that a variant of a virus manages to evade defenses by mutating significantly, but those mutations to also make it weaker due the randomness of what is needed to do so at any point. But it’s not a guarantee, and I don’t think science can even tell what those are (outside of the first line), let alone probabilities due to the complexity of the host and of testing all of the protections.
What if the virus binds at moderate affinity to the target, and by mutation the binding becomes stronger?
There’s no reason to have some trade off . Most of the time mutations that make the virus spread less easily are selected against.
JonRowe
1909
lol
I would disagree with your thoughts on it being a living organism per se. That is debatable.
But the objective of a virus is to reproduce and make more of itself, that is the only goal. The fact that it causes illness in us is just a byproduct of the mechanisms and cells that it targets.
The basic facts are, the better it can reproduce, the better the virus. Killing hosts is not something that makes you more able to reproduce, so usually those mutations and variants go away, and the more transmissible ones that in turn cause lighter illness stick around. This is how other common cold style coronaviruses that also attack the upper respiratory system work.
The example of rabies is different, as it is a rhabdovirus, and it is also not super transmissible, so the host pool is pretty small for evolution. It is possible that in 10,000 years rabies is no longer fatal, who knows?
