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by mlyle 2199 days ago
This is a good introductory treatment of the topic:

https://www.medrxiv.org/content/10.1101/2020.04.27.20081893v...

> well that speed changed already much earlier

Your comment is a bit self-contradictory and muddled. That is, we're talking about the herd immunity threshold under baseline behavior; what percentage of the population needs to have been infected to result in infections decaying with original behaviors.

The point I was making is that it seems like case counts are decaying much quicker in regions with high seropositivity than other regions with similar regulations and similar empirical measures of mobility. This would imply that under current conditions even the modest immunity reached seems to make a bigger difference than naive assumptions about immunity and resulting Rt imply.

We already know that contact networks are not uniform (source: duh); further, individual susceptibility apparently varies significantly (from genetic studies). These factors significantly change the percentage that must be organically infected to reach herd immunity.

It's worth noting that this difference has both optimistic and pessimistic implications. Optimistic: regions that have high seropositivity are more likely to have the worst behind them. Pessimistic: the amount of vaccination to have equal effect probably far out-strips current seropositivity rates, because it can't effectively be targeted based upon susceptibility and network structure.

1 comments

I tried but I don’t see that the paper proved anything about the current pandemics?
A paper doesn't "prove" anything, but it does utilize and cite upon real world mobility data and real world susceptibility and transmissibility data for many diseases, including early estimates of these for SARS-CoV-2, e.g. https://wellcomeopenresearch.org/articles/5-67 is cited and used in the estimate of the coefficient of variation.

There was very little data on overdispersion and differential susceptibility for SARS-CoV-2 at the time that paper was written, but there was some. What existed at the time was in line with the better estimates from SARS-CoV-1, etc, that the paper also used. Further evidence has emerged since, both of variable susceptibility and exposure and of actual mechanisms of variable susceptibility-- some surprising like https://www.medrxiv.org/content/10.1101/2020.04.08.20058073v...

Good, so we agree that nobody has proved for SARS-CoV-2 that less than 70% of can be infected to achieve the so-called "herd immunity" (even when knowing that different people allow some very lax definitions of "herd immunity").
Yes, and nobody has proven really -anything- about most things, by this metric. All we have is evidence of varying quality.

But, again: it's pretty much settled science that Rt = 1 when 1-(1/R0) is infected is a worst case not very often attained, and the evidence so far with COVID-19 (looking at time series data, evidence of non-uniform susceptibility, clear evidence of non-uniform contact networks, significant evidence of overdispersion, etc) leans strongly that way.

Bigger issue is: if 25% infected yields expected Rt of under 1 (the threshold for herd immunity, and I think this is likely)... you'll still have a fair number of cases, because people will come from other jurisdictions with the disease and it'll trigger chains of spread that only slowly decay / peter out each time. If you're one of the other 75%, you're hardly safe, because you can be exposed to one of these chains. Only vaccination can address this, and it's not even a complete fix.

> if 25% infected yields expected Rt of under 1 (the threshold for herd immunity, and I think this is likely)

That's what I'm missing, what are your sources to think that? I somehow haven't seen that in the links you gave.

From the very first link:

> The herd immunity threshold (HIT) defines the percentage of the population that needs to be immune to reverse epidemic 15 growth and prevent future waves. Figure 3 shows the expected downward trends in the HIT for SARS-CoV-2 as the coefficients of variation of the gamma distributed susceptibility or exposure are increased between 0 and 4 (to assess robustness to changing the type of distribution see Figure S22 for equivalent plots with lognormal distributions). While herd immunity is expected to require 60-70% of a homogeneous population to be immune given an R0 between 2.5 and 3, 20 these percentages drop to the range 10-20% for CVs between 2 and 4.

Curvefitting from COVID-19 incident waves, past SARS experiences, surveying of contact tracing data, pre-epidemic mobility data in the population, etc, all point to CVs around 3 which corresponds to a herd immunity threshold of 15% or so (hence the paper's 10-20% range). I think this is optimistic and a threshold of more like 30-35% is likely, which with durable aspects of behavior change might really end up being ~25%.