How long until herd immunity?

So, we’d all hoped that enough people would be vaccinated to bring us to herd immunity. And, well, I think it’s clear by now that that’s not going to happen. But while vaccination is the best route to herd immunity, it’s not the only one: Sooner or later, everyone who’s going to get the shot will get it, and everyone who’s trying to get infected will succeed. And so, eventually, this pandemic will end (albeit with a lot more suffering than necessary along the way).

Are there any estimates out there for how long this will take? It’s complicated, I’m sure, by the fact that pro-vaxers tend to congregate with other pro-vaxers, and anti-vaxers with other anti-vaxers, but I’m sure that epidemiologists have models for that sort of thing.

One complication is that immunity doesn’t last forever. While those of us who are vaccinated will continue getting boosters, the antivaxxers won’t.

I’m not sure how that plays with the numbers.

Fourth wave starting in Europe. Might not take as long as we’d feared, albeit by a mechanism we never anticipated. Can’t fix stupid, but apparently you can get it to kill itself with its own stupidity in huge numbers.

That’s a magnificently positive spin to put on it!
Have you considered a career in PR or the church? :upside_down_face:

Immunity (whether acquired thorugh infection or vaccination) for most pathogens does not last “forever”, i.e. for a person’s lifespan. The common interpretation of “herd immunity” as some point at which a pathogen essentially disappears from circulation is just not correct; from an epidemiological standpoint, “herd immunity” is just the point at which enough of a population is sufficiently resistant that it is no long possible to sustain an epidemic level outbreak and the pathogen becomes endemic in the population; that is, that the effective replication number is consistantly below unity across the population.

For some pathogens this occurs naturally; seasonal Influenza A, for instance, tends to burn through an uninnoculated population until replication falls below the epidemic threshold, and then becomes endemic until it mutates or combines with another variant to develop into a new strain. Prior to comprehensive vaccination, the poliovirus responsible for poliomyelitis tended to fluctuate betwen epidemic and endemic. Varicella zoster, responsible for chickenpox, has never fallen below epidemic thresholds even though prior to a vaccine virtually every adult on the planet was exposed and had acquired immunity sufficient to prevent recurrence (in the chickenpox form, although the virus is resident in the dorsal root ganglion of sensory nerves and can reemerge to cause shingles in patients under high stress or with various autoimmune conditions).

For SARS-CoV-2, the acquired immunity through infection does not seem to provide very robust protection; at three months post-infection it appears to provide somewhere around 60% protection from reinfection, compared to between 80% t0 95% for most two shot vaccines (mRNA and adenovirus vectors), and falling dramatically thereafter. Even worse, about 1 in 5 in natural infection do not develop antibodies against either the S-protein or the nucleocapsid protein; whether that is luck of the draw or some kind of persistent genetic issue is unknown, but it appears there will be a substantial population of people who will probably not acquire natural immunity despite repeated exposures and will provide a reservoir for future infection. Vaccines appear to provide a more resilient antibody response, and it may be that with a longer sequence of vaccinations (3 or 4 shots, perhaps spread over a period of many months or even a couple of years) could provide lasting immunity, at least against the current strain of the virus.

Frankly, this pathogen is transmissible enough and capable of regular mutation that there is no reason to expect that it will ever disappear from circulation. What will likely happen is that eventually a variant will evolve that is infectious enough to outcompete other variants but only marginally pathogenic (causing only mild and transient respiratory issues, similar to other “common cold” viruses), thus preventing more pathogenic variants from taking hold. Of course, the opposite could also occur; SARS-CoV-2 could mutate to become as pathogenic as SARS-CoV(-1) or MERS-CoV, with double digit mortality rates, and potentially into a novel strain resistant to current antibodies, in which case this current pandemic would just be a light precursor to the main event of truly catastrophic proportions. This is one reason why there needs to be a system of worldwide monitoring of infection and sequencing of a statistical sampling to identify potentially threatening strains before they cannot be contained. (We also need to monitor the virus in the many animal reservoirs it is known to live in, because even though there has not yet been an instance of spillback from domestic or game animals, and the spillback incident from farmed mink was not more pathogenic than the wild-type virus, it is probably a matter of time before a more virulent variant emerges from another animal reservoir, and we can only hope that it is not as infectious as currently circulating varianrts.)

Although a lot of focus has been put onto “herd immunity” as a resolution to the pandemic, particularly in the popular press, in epidemiological and especially immunological circles more focus has gone into harm abatement, e.g. getting as many people vaccinated as possible, even with the less effective vaccines with waning immunity (which, it should be noted, are still quite effective in preventing severe disease and death) as well as developing theraputics to treat infected patients such that they do not require intensive and invasive treatments. The pandemic will be effectively over when this disease can be treated by prescribing a standard course of retroviral treatments and/or limited through comprehensive vaccination, but the expectation that this will just somehow disappear isn’t realistic, and it isn’t likely that it could be completely eradicated even by a global campaign like that which eradicated smallpox, rinderpest, or (almost) polio.

Stranger

Apparently, COVID is running pretty rampant in deer populations. Cats can also get it and transmit it (dogs appear to be better at not getting or spreading it). Will animal reservoirs keep this thing going?

Human reservoirs seem to be doing fine at perpetuating the virus, especially since even people who have been fully vaccinated with mRNA and adenovirus vaccines have been shown to be able to contract and spread the virus even when they are asymptomatic. I don’t believe any spillback has been shown from domestic animal (cat, dog, et cetera) but the potential certainly exists since the virus has been observed to infect numerous mammalian hosts. The MERS-CoV virus (a betacoronavirus like SARS-CoV-2 but of lineage Merbecovirus) is quite readily able to pass from camels (where it is only mildly pathogenic) to humans (where it has an estimated infection fatality rate of >30%) so it is not inconceivable to that SARS-CoV-2 could spill over to an animal host and evolve to become more pathogenic, and then spillback.

Of course, it is also possible that MERS-CoV could become better adapted to humans and more readily transfer from person-to-person, or the original SARS-CoV(-1) could return from wherever it came from initially, or that something like the Nipah henipavirus could become more transmissible, or just the really serious Influenza A pandemic that epidemiologists have been warning that we are overdue for for the last several decades. Given the sparse monitoring and cooperation between national health authorities, there are plenty of threats that could hurricane through the global population that would make the current COVID-19 pandemic look like a mild rain shower in comparison,.

Stranger

Fantastic. Thanks for the uplifting post.

“This is the room for Cynicism. If it is Sangunicity you are looking for, check with Mr. Slattery in 12A.”

Stranger

Cite for this? Everything I’ve seen is that immunity from actual infection is stronger than from the vaccines (though of course having both is even stronger yet).

And a cite for this, too? From what I’ve read elsewhere, even though it mutates readily, it probably won’t mutate in such a way as to be able to evade the vaccines.

That article’s behind a paywall. Does it attempt to explain how deer, who traditionally don’t spend much time indoors, are becoming infected?

Here’s the original study: https://www.biorxiv.org/content/10.1101/2021.10.31.466677v1

Here’s the a useful quote from the Times article:

A new study of hundreds of white-tailed deer infected with the coronavirus in Iowa has found that the animals probably are contracting the virus from humans, and then rapidly spreading it among one another, according to researchers.

That leaves me with more questions than answers. I’m picturing humans coughing, sneezing, or yelling in deer’s faces, which I wouldn’t think happens that often.

Are there any studies on herd immunity that factor in deliberate sabotage?

I couldn’t understand why the continued re-emergence of the virus against an ever increasing immunity both from vaccinations and natural immune response.

I think this article might explain it..

This is not like the flu virus because of the way it replicates. It is much more prone to variations and that might be why it will never go away.

Here in my state NSW we are up to 91.4% fully vaccinated, 94.3% first dose, of the population >12yo as of yesterday. So if herd immunity is a real thing, we should pretty much be there.

OTOH they are already planning booster shots and vaccines for the 5-12 cohort next year, and today I saw my first mention of a possible need for a second booster shot …

Since this was bumped, I’ll make a stab. Scientists have been saying that herd immunity can’t be reached even before the delta variant swept through. However, they were talking about some kind of return to normal. Some things I’ve been thinking about.

  • Normal means that waves don’t get so bad that emergency rooms and surgery/procedure scheduling won’t be hindered by a surge of covid patients.
  • If the delta was as contagious as chicken pox, this would require about 85% of the population (including kids) being vaxxed (with an mRNA or boosted if J&J+mRNA) or previously-infected.
  • What countries to follow? Portugal is highly-vaxxed (87%) with a good number of previous infections. Israel and UK are not highly-vaxxed (67%/62%) but highly-boosted with tons of previous infections. Denmark, Australia, and Japan are pretty well-vaxxed (~ 75%) but have fewer previous infections (Japan hardly any). Then there’s the US and Brazil middling vaxx rate but high infections. There’s plenty more, but that’s what I’m looking at.
  • Boosters: strength and longevity. So far, Pfizer boosters increase antibodies beyond levels seen two weeks after the second shot. So stronger immunity? Will this also increase longevity?
  • Models are suggesting milder winter surge that peaks later than last winter’s. However, they already seem to be missing a turnaround of cases happening right now in the US.
  • How much more can the virus mutate to increase transmissibility/replication/immune evasion?

I don’t know if this will answer your question but here’s a cite from Dr Stappenbeck of the Cleveland Clinic discussing the nature of covid replication vs other viruses.

to summarize what he said. the original strain of the virus would spread from one person to 2 others. The Delta strain now moves from one person to 10 others.

The method of how the virus works is also described and this is a quote:
Yeah. So it really depends on the types of viruses. So influenza has a bunch of different genes that kind of recombine with each other and form different strains. The SARS viruses are RNA viruses, and this is a little different. So these are RNA viruses, these viruses replicate when they get inside of our cells. There are certain types of viruses called DNA viruses, where they use our replication machinery that we use to have our own cells divide to make copies of themselves. And because of that, the copies don’t have that many mistakes. RNA viruses use their own machinery, they encode their own machinery to make replicates of themselves. And these replication machineries are very prone to errors.

I find this quote strange. Flu viruses are also RNA viruses:

And coronaviruses are less susceptible to mutation than other RNA viruses because of error correction:

Coronaviruses are genetically more stable [than influenza and HIV] because they carry within them a mechanism for correcting errors that naturally occur through mutation of their genetic code. The genomes of HIV, flu, and coronavirus are all made of RNA, which is less stable and more prone to error than the DNA that stores our own genetic information. All three viruses mutate because they rely on RNA, but coronaviruses do so more slowly.