1/X

Those behind the Great Barrington Declaration mention herd immunity as a way to address COVID-19.

So I'll discuss it. After all, noting herd immunity (in response to vaccine deniers) is 1 main reason I started on Twitter.

https://twitter.com/AtomsksSanakan/status/891040491214688257

https://gbdeclaration.org/ 
2/X

Suppose u want to know how many people would die from COVID-19 under *baseline conditions*.

So basically: treat COVID-19 like another typical disease, with business-as-usual and acting the same as this time last year without the pandemic. https://twitter.com/AtomsksSanakan/status/1337238156052226050
3/X

Re: "how many people would die from COVID-19 under *baseline conditions*"

One can figure that out using:
- the number of people who would get infected
- how many of those infected people die of COVID-19

A separate thread on the latter point: https://twitter.com/AtomsksSanakan/status/1341443629349543937
4/X

The virus infects more people if the virus is more contagious, meaning it has a larger R0.

R0 of 2 implies each infected person infects 2 other people on average, at baseline, before they stop being infectious.
For R0 of 3, they infect 3 others.
Etc

https://www.mdpi.com/2076-393X/8/2/236/htm
5/X

Eventually, so many people become non-infectious + immune to infection, that the virus struggles to find non-immune people to infect and use to infect other non-immune people.

That's the idea behind herd immunity.

https://medium.com/@silentn2040/the-dangerous-myth-that-sweden-achieved-herd-immunity-fd2579526b8b
6/X

The 'herd immunity threshold' (HIT) is the proportion of people who need to be immune to infection, in order for 'infections per unit time' to stop increasing (i.e. keep R under 1), at baseline.

At HIT, the outbreak is on its way to dying out. https://twitter.com/AtomsksSanakan/status/1309297907863035904
7/X

The classic calculation for HIT is:
1 - (1 / R0)

So an R0 of 3 implies:
HIT = 1 - (1/3) = 67%

A larger R0 means a larger the HIT.

In other words: a more contagious virus means more people need to be immune to infection for the outbreak to die out.

https://www.sciencedirect.com/science/article/pii/S1074761320301709
8/X

Different places have different baseline conditions, + thus different values for R0 and HIT.
https://www.journalofinfection.com/article/S0163-4453(20)30154-7/fulltext

A typical R0 for a western country is ~2.5 or more, implying at HIT of >= 60%. Higher than seasonal flu.
https://link.springer.com/article/10.1186/1471-2334-14-480

https://www.thelancet.com/action/showPdf?pii=S1473-3099%2820%2930484-9
9/x

People still get infected after HIT is reached, but not enough to replace the people who become immune after they recover from infection (since R is now less than 1).

This implies "overshoot": the final percentage of people infected is more than HIT

https://twitter.com/CT_Bergstrom/status/1252009362849009664
10/X

So for the question from part 2/X:

How many people would die from COVID-19 under *baseline conditions*?

Ferguson et al. answered this in March, with a HIT of ~58%, and IFR of 0.9% for Great Britain (~0.8% for the USA):

https://twitter.com/AtomsksSanakan/status/1337273174967394305

http://web.archive.org/web/20200421012308/https://spiral.imperial.ac.uk:8443/bitstream/10044/1/77482/14/2020-03-16-COVID19-Report-9.pdf
11/X

So how does this play out in reality?

Well, a respiratory virus like SARS-CoV-2 that spreads by droplets + aerosols, takes longer to infect a given proportion of people in:
- a larger population
- a population spread over a wider geographical area https://twitter.com/AtomsksSanakan/status/1292997236843057156
12/X

Since SARS-CoV-2 is very contagious (high R0 and therefore high HIT), SARS-CoV-2 then quickly infects a large proportion of people in smaller populations and/or populations covering small areas, before behavior changes and interventions limit spread

https://twitter.com/AtomsksSanakan/status/1293007098134044672
13/X

SARS-CoV-2 also infects a higher proportion of people in areas that remain closer to the baseline conditions of R0 (i.e. not much infection-limiting behavior changes and/or public health interventions like mask-wearing).

https://twitter.com/AtomsksSanakan/status/1323672387121020930

https://web.archive.org/web/20201102030724/https://www.researchgate.net/publication/343414173_Seroprevalence_of_anti-SARS-CoV-2_antibodies_in_the_city_of_Iquitos_Loreto_Peru
14/X

Larger populations see people dying of COVID-19, and respond with additional behavior changes + public health interventions that push them further from the baseline conditions of R0.

That limits the spread of SARS-CoV-2 and limits COVID-19 deaths.

https://twitter.com/AtomsksSanakan/status/1338578097013219339
15/X

So larger populations and/or populations spread over larger geographic areas, end up with a lower proportion of people infected, even though HIT is high.

Some people see those lower proportion of infected people, and incorrectly infer HIT is low

https://twitter.com/AtomsksSanakan/status/1283817701316714499
16/X

But remember, it wasn't herd immunity that limited infections into larger populations and regions; those regions didn't reach HIT.

Instead, it was behavior changes and/or public health interventions that limited infections

https://twitter.com/AtomsksSanakan/status/1337362849820266500

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7289569/
17/X

I'll make a claim some people may find controversial:

Claiming HIT is very low (ex: ~10% - ~20%) is *dangerous and obviously incorrect.*
In fact, it may be the most dangerous idea to emerge during the COVID-19 pandemic.

https://twitter.com/AtomsksSanakan/status/1337240769732767744

https://twitter.com/AtomsksSanakan/status/1337255624854425600
18/X

Saying we reached a low HIT tells us we no longer need to go beyond *baseline conditions* to prevent infections/day from increasing; i.e. no additional:

- mask-wearing
- avoiding visiting nursing homes + large indoor gathers
- vaccinations
etc.

https://twitter.com/AtomsksSanakan/status/1292337005918068736
20/X

The non-experts have no background in epidemiology, immunology, etc.

So they falsely assume only herd immunity can limit R and thus limit infections per day; i.e. they assume if infections/day and COVID-19 deaths/day decrease, then HIT was reached

https://archive.is/h96zK#selection-23077.0-23105.283
21/X

But factors other than herd immunity can limit infections and deaths, as covered in part 16/X. So the non-experts are wrong.

You can usually spot these non-experts because they claim Stockholm, Sweden (or New York City, or...) reached HIT.

Yet...
https://archive.is/CKncm#selection-17975.0-18009.608
22/X

So what about experts who claim HIT is low? Probably the most well-known one is Gabriela M. Gomes ( @mgmgomes1).

Unlike the non-experts, her team is aware that HIT is about baseline conditions of R0.

https://twitter.com/AtomsksSanakan/status/1337240276356751361

https://www.medrxiv.org/content/10.1101/2020.09.26.20202267v1

https://www.medrxiv.org/content/10.1101/2020.04.27.20081893v3.full.pdf
23/X

But the expert proponents of low HIT still need to distinguish the effects of HIT, vs. the effects of behavior changes + public health interventions.

Turns out Gomes' team did that incorrectly.

https://twitter.com/FoxandtheFlu/status/1334546142852337664

https://www.medrxiv.org/content/10.1101/2020.12.01.20242289v1.full.pdf
24/X

When one better accounts for the effects of behavior changes + public health interventions, HIT is >50% (green), instead of ~10% - ~20% (blue).

Achieving this higher HIT, without a vaccine, would cause more COVID-19 deaths.

https://twitter.com/AtomsksSanakan/status/1337217585377660928

https://www.medrxiv.org/content/10.1101/2020.12.01.20242289v1.full.pdf
26/X

Why think HIT is high?

One reason centers on heterogeneity vs. homogeneity.
Or in layman's terms: differences vs. sameness.

The "HIT = 1 - (1 / R0)" calculation from part 7/X assumes sameness, while low HIT proponents claim large differences.

https://www.sciencedirect.com/science/article/pii/S1074761320301709
27/X

If "heterogeneity vs. homogeneity" is confusing, think of a sexually-transmitted infection (STI) like HIV.

With STIs, heterogeneity is high (so large differences virus transmission interactions).

https://twitter.com/bansallab/status/1259970552074207238
https://cambridge.org/core/services/aop-cambridge-core/content/view/C24D3E55E075B29059AF654BB6D84576/S1446181113000035a.pdf/spatial_heterogeneity_in_simple_deterministic_sir_models_assessed_ecologically.pdf

https://archive.is/qBEuG#selection-19093.0-19093.887
28/X

But SARS-CoV-2, the virus that causes the disease COVID-19, isn't an STI. It's a respiratory virus spread by droplets + aerosols, using behaviors more common to everyone, such as breathing + face-touching

So there's more sameness (i.e. homogeneity)

https://www.quantamagazine.org/the-tricky-math-of-covid-19-herd-immunity-20200630/
29/X

Ironically, many non-experts try to lecture me on how heterogeneity (differences) are large for SARS-CoV-2, when they know less about this than me. 🤦‍♂️

Highlights in tweets in part 30/X onwards, in case they try this on you.

https://twitter.com/VicenteAriztia/status/1289397995092484096

https://twitter.com/AtomsksSanakan/status/891040491214688257
30/X

Different T cell responses between people won't give enough heterogeneity to greatly lower HIT, especially since T cells are not primarily involved in limiting infections. They're more about responding after infection.

https://twitter.com/profshanecrotty/status/1309170532965920769

https://twitter.com/AtomsksSanakan/status/1309311345947484166
31/X

In layman's terms: cross-reactivity involves the immune system treating SARS-CoV-2 like another virus the immune system previously responded to, such as another coronavirus.

Cross-reactivity isn't going to drop HIT by a lot

https://twitter.com/AtomsksSanakan/status/1312654302742183936

https://www.nature.com/articles/s41577-020-00460-4
32/X

There are transmission differences, such as medical professionals generating aerosols when they intubate people (i.e. place tube down their throat), placing those professionals at more risk from SARS-CoV-2-containing aerosols.

http://web.archive.org/web/20201223222714/https://apps.who.int/iris/bitstream/handle/10665/331601/WHO-2019-nCoV-Sci_Brief-Transmission_modes-2020.1-eng.pdf?sequence=1&isAllowed=y
33/X

But these differences occur for other respiratory viruses such as influenza, w/o causing a much lower-than-expected HIT.

Other pertinent differences are likely already included in R0 (see parts 28/X and 31/X).

https://twitter.com/AdamJKucharski/status/1294985964801142784

https://archive.is/8MiEc#selection-19555.0-19559.843
34/X

There isn't perfect sameness (perfect homogeneity).

But it's homogenous enough for a high HIT + to have "HIT = 1 - (1 / R0)" from part 7/X be a decent approximation, consistent with the high infection rates from 12/X + 13/X

https://twitter.com/AtomsksSanakan/status/1339263966678224897

https://www.medrxiv.org/content/10.1101/2020.12.01.20242289v1.full.pdf
35/X

Proponents of low HIT also predicted areas with high infection rates wouldn't have strong second waves.

They were wrong (another example in part 21/X).

https://twitter.com/OYCar/status/1318386897660518401
https://twitter.com/akcayerol/status/1318376173177606151
https://twitter.com/mikejohansenmd/status/1320453089875447810

https://archive.is/m8e89#selection-22359.0-22889.33
https://twitter.com/thomdvorak/status/1319657564003500032
36/X

Gomes' low HIT framework predicted places with higher infection fatality rates would have lower infection rates.

That didn't consistently hold up.

https://twitter.com/mgmgomes1/status/1310944207901687810

https://www.mdpi.com/2079-7737/9/6/128/htm
https://web.archive.org/web/20200830215825/https://www.preprints.org/manuscript/202008.0648/v1

https://twitter.com/AtomsksSanakan/status/1333154830962094088

https://twitter.com/GidMK/status/1277804390603059201
37/X

The observed pattern of infections and COVID-19 deaths better fit one would expect from behavior changes + public health interventions limiting infections, not herd immunity (with a low HIT) limiting infections, as per part 16/X.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7289569/
38/X

There are other region-specific reasons to think particular regions did not reach a low HIT. I've covered some elsewhere:

https://twitter.com/AtomsksSanakan/status/1282213024905015298

https://medium.com/@silentn2040/the-dangerous-myth-that-sweden-achieved-herd-immunity-fd2579526b8b
39/X

So some reasons for thinking the herd immunity threshold is high:

- the biology underlying transmission of respiratory viruses
- high infection rates
- second waves
- higher fatality rates at higher infection rates
etc.

And I've see no good reason to think HIT is very low
40/X

Some folks claim HIT is low, b/c it allows them to downplay how dangerous COVID-19 is + thus avoid policies they dislike (like lockdowns).

Hence why many of the same people who suggest HIT is low, also under-estimated SARS-CoV-2's fatality rate. 🤷‍♂️

https://twitter.com/AtomsksSanakan/status/1314397925016064000
41/X

Also, other factors can increase HIT.

For example: people not becoming immune to infection after they're infected. The "HIT = 1 - (1 / R0)" calculation assumes persistent immunity after infection, as per part 26/X.

https://twitter.com/AtomsksSanakan/status/1316757724387041285

https://archive.is/Xjyec#selection-15423.0-15455.142
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