Shouldn't we limit the vaccines for the risk populations in that case? Vaccinating everybody just promotes vaccine resistant variants.
* Hiding this fact is a serious problem of the 'never name a mutation by a place' new WHO policy.
Considering that even the most highly vaccinated places on earth are shattering records of infection rates, it seems implausible that vaccinating the rest of the world would somehow fix this issue. The "most unvaccinated" places on earth are also some of the most populous, therefore a variant is most likely to arise there out of pure chance.
In this case, due to the large number of mutations, the prime suspect is an untreated HIV patient with a lingering infection, which is most likely to happen in the southern parts of Africa. It's not clear whether vaccines prevent lingering infection in such a case.
OP was suggesting intentionally limiting vaccination. If 'natural' immunity can also allow for antibody-evading mutations, than we get nothing from limiting vaccinations - my point exactly.
>Considering that even the most highly vaccinated places on earth are shattering records of infection rates, it seems implausible that vaccinating the rest of the world would somehow fix this issue.
We cannot make mutation never happen, but we can limit the damage by vaccinating more. This will help us gain time to get more effective medications.
No, that doesn't follow. Vaccines target a spike protein specifically, hence selecting for a variant that defeats that particular kind of immunity, making vaccines obsolete for those that need them the most. This is a hypothetical vaccine-escape variant, not this Omicron variant. We know nothing about its actual capability for vaccine-escape.
Natural immunity targets the whole virus, so whatever immune-escape such a virus evolves, it would have to be far more comprehensive to have a significant effect. We may or may not have that in this particular variant and we're still at the very beginning of that wave:
https://pbs.twimg.com/media/FFGNLl3XMAsNQXE?format=jpg&name=...
A virus avoiding spike antibodies would have an advantage whether these antibodies were 'natural' or not, so it's far from clear natural immunity wouldn't lead to the same mutations - all the VOCs hail from mostly unvaxed countries, which leads to the suspicion that it does.
Sure, the 'naturally immune' sick people having extra N-targeting antibodies would be in an advantage vs the virus, but the cost of that is having a real corona infection earlier on, with all the risk simply being frontloaded.
* EDIT: the Chinese vaccines are inactivated virus vaccines. One wonders whether they fare better or worse vs this variant. Then again, maybe this variant will fail to transmit effectively and will just kill itself off like Beta did.
> Sure, the 'naturally immune' sick people having extra N-targeting antibodies would be in an advantage vs the virus, but the cost of that is having a real corona infection earlier on, with all the risk simply being frontloaded.
It's not a binary, when people get vaccinated and then infected (or vice versa), they do develop broader immunity. Frontloading the risk of infection versus vaccination may well be justified in the young and healthy population, but that opinion has been ostracized from the mainstream.
> the Chinese vaccines are inactivated virus vaccines. One wonders whether they fare better or worse vs this variant.
Not all of them are, but CoronaVac is. This[1] suggests that while efficacy of CoronVac against wild-type infection was modest (51%), the reduction when confronted with Gamma was very small (49.6%).
> Then again, maybe this variant will fail to transmit effectively and will just kill itself off like Beta did.
Beta didn't "kill itself off", it led to wave that rivaled Delta/Gamma in some cases. It ended up being outcompeted by Delta/Gamma.
[1] https://www.who.int/news-room/feature-stories/detail/the-sin...
There isn't. We have to theorize on the move, so to speak.
>Frontloading the risk of infection versus vaccination may well be justified in the young and healthy population, but that opinion has been ostracized from the mainstream.
The problem is that people took the wrong assumptions when calculating the risk of disease. All our calculations of risk are based on hospital treatment being available: providing Oxygen, Dexamethasone and ECMO treatment to critically ill patients, and no extra deaths due to healthcare overload.
No scenario when we 'let it rip' involves being able to give Oxygen to all young people who need it, and there will be extra deaths due to overload. The clever people suggesting intentional infection assumed risk factors dependent on current policies without understanding that under their policies risk would shoot up.
>Beta didn't "kill itself off", it led to wave that rivaled Delta/Gamma in some cases. It ended up being outcompeted by Delta/Gamma.
That's functionally equivalent to 'killing itself off', or at least being much less of a threat. I recall Beta's transmission factor was lower than Alpha? Was it because it missed some key mutations, or because mutating to avoid immunity came with a cost?
This is highly speculative. Considering the exposure and infection rates among the younger population, particularly those of school age, can't we say we did let it rip? Infection seroprevalence in blood-donors was at 20% by July[1]. How much worse could it possibly be?
https://jamanetwork.com/journals/jama/fullarticle/2784013?al...
(Ominous music)
>Infection seroprevalence in blood-donors was at 20% by July[1]
Seriously though, two points:
A) I have doubts about this measurement - that level (83.3% with antibodies!) should have been enough for herd immunity in May 2021, yet we don't see it in the US, cases being broadly static in the last month*.
Perhaps American blood donors are highly nonrepresentative even after demographic adjustments? Or they're catching people with very low levels of antibodies but without true immunity? The paper is thorough regarding geographic and demographic factors, but isn't very clear on the technical details of the measurement itself beyond 'we did it, here are the results'.
Or we could argue the US had herd immunity in May yet lost it two months after, that's not very encouraging, not even for 'natural' immunity.
B) Assuming the researchers are correct, that's 20% for over a year. That's very different from having it way quicker.
>can't we say we did let it rip?
School closures, remote learning, masks even at that age. Obviously there have been (arguably way overzealous) efforts at controlling COVID even at the youngest ages.
* There's a very recent fall, it's probably reporting lag - or it's really down, but per the research that should have already happened long ago.
The 83% includes immunity from vaccination which, as we know now, is not sufficient for herd immunity. Natural immunity may not be sufficient either.
> School closures, remote learning, masks even at that age. Obviously there have been (arguably way overzealous) efforts at controlling COVID even at the youngest ages.
In many cases, schools didn't get closed during much of the Delta wave and incidence in the young population was particularly high. As for masks: They have a modest effect at best (20% risk reduction).
I never thought about it that way. That would mean, if the virus evolves a more efficient ACE-2 binding domain that the mRNA vaccines fail to recognize, the vaccinated population would be more at risk than the unvaccinated population who has been previously exposed.
"Geneticists and infectious disease specialists there have uncovered potentially dangerous coronavirus mutations in a 36-year-old woman with uncontrolled HIV who was unable to shake the SARS-CoV-2 virus for close to eight months."
That was reported back in June:
https://www.latimes.com/science/story/2021-06-03/why-reachin...
[2] https://www.ft.com/content/06334a7b-30cc-40bf-942b-e3bcd2efb...
[0] https://www.theguardian.com/world/2021/nov/26/vaccine-resist... [EDIT]
The fact that most VOCs popped in areas with little to no vaccination coverage quite aligns with that.
For omicron the main hypothesis is it actually evolved in a severely immunocompromised HIV patient.
Edit:
This isn't exactly new[0] and it's also been witnessed for SARS-CoV-2[1]:
> These compilations of case reports indicate the need to identify whether certain forms of immunosuppression are associated with an increased risk of such multimutational escape patterns — for instance, specific cancers or specific therapies, such as the development of B-cell aplasia related to CAR T-cell or anti-CD20 therapy, prolonged use of glucocorticoids, long-term chemotherapy, or radiotherapy. Similarly, organ transplant recipients and those with untreated or poorly controlled human immunodeficiency virus infection may also have prolonged SARS-CoV-2 infection and could constitute a reservoir of divergent escape variants that can spread in the general community. Prolonged viral replication in the context of an inadequate immune response facilitates the emergence of immune-pressure escape mutations.[0]
I'd appreciate an actual counter argument, other than a poorly understood Marek disease analogy.
SARS2 mutates much more slowly than Influenza so, IMO, we actually NEED to get people more infected. I would not be saying this if we locked every country down in the beginning but this is where we are.