Trevor Bedford ✓
@trvrb · Seattle, WA · joined 10 Dec 2010
Scientist @fredhutch, studying viruses, evolution and immunity. Collection of #COVID19 threads here: https://t.co/Yc4fun5rcp
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Procurando novos posts…
Currently, the US is reporting about 54k daily cases of COVID-19 (16 per 100k per capita) and the UK is reporting about 4k (6 per 100k). This seems comfortingly low compared to even this summer's BA.5 wave and let alone last winter's BA.1 wave. Figure from @OurWorldInData. 1/16 h
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I was invited by @VandammeAm and other organizers of the #VEME2022 Virus Evolution and Molecular Epidemiology Workshop to present my perspective on applying pathogen phylogenetics for decision making. Slides from my talk are available here: https://t.co/dcRz1LSpbP.
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Largely through partial immune escape, lineage BA.5 viruses resulted in sizable epidemics throughout much of the world. However, in most countries these epidemics are now beginning to wind down. What do we expect after BA.5? 1/10 https://t.co/zze4p5ebEJ
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Follow up #1: I had missed this thread by @C_Althaus previously. It nicely demonstrates similar results in terms of dampening seasonal oscillations with increasing waning / antigenic drift.
https://t.co/HvGhrBK2wE
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@trvrb Very interesting! Do I understand correctly that:
Faster waning due to faster immune evasion compared to flu could make it less seasonal than flu even in the long run
Or, what we're seeing could be closer to the "end state" than what one may think based on naive comparison
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I'm not trying to make a prediction here, but just illustrate a scenario where we end up in a regime of year-round variant-driven circulation with more circulation in the winter than summer, but not flu-like winter seasons and summer troughs. 11/11
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If what we've seen with Omicron evolution in 2022 becomes largely the norm, then this result would imply waning of ~24% in the span of ~6 months, or very roughly waning from R→S on a ~1.8 year time horizon, ie close to the yellow curve in the above SIRS model. 10/11 https://t.co/
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Although it's difficult to estimate long-term rate of R→S for SARS-CoV-2, we can extrapolate from @HebAltarawneh et al's finding of 76% effectiveness of BA.1 infection to prevent BA.4/BA.5 reinfection (https://t.co/tPcceilmmk). 9/11
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Even outside of emergence of wildly evolved Omicron virus, we've so far seen faster evolution of SARS-CoV-2's spike protein relative to influenza H3N2's equivalent HA1 protein. 8/11 https://t.co/rKk1nQbOBf
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Here, we see that with flu-like ~5 year rate of waning (in blue), we get winter epidemics and summer troughs, while with faster waning we see greater levels of circulation and less variation between winter and summer (in yellow and red). 7/11 https://t.co/VZ2HOvLpQM
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Including seasonal forcing for seasonal influenza where R0 is a bit lower and rate of waning / antigenic drift restores R→S every ~5 years, we get slow build up of susceptibility over the summer that followed by winter forcing results in winter epidemics and summer troughs. 5/11
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However, if waning / viral evolution is fast enough, then this can drive summer circulation and reduce build up of susceptibles. We can see this by running SIRS models with different rates of waning, but otherwise largely SARS-CoV-2-parameters. 6/11
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As @adamjkucharski expresses here, with SARS-CoV-2-like intrinsic transmissibility (with R0 of circulating viruses of perhaps ~8), infections will be largely gated based on speed of immune waning / viral evolution. 4/11
https://t.co/qGwjtct7rg
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In particular, we can use an SIRS system in which individuals go from Susceptible to Infected to Recovered, and then return to the Susceptible class due to immune waning / antigenic drift of the virus. 3/11
https://t.co/jnqdHUBVH5
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It's necessarily fraught to try to make predictions of seasonal circulation patterns going forwards, but we can gain some intuition from simple epidemiological models. 2/11
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Based on the experience in winter 2020/2021, seasonal influence on SARS-CoV-2 transmission is quite clear, but much of the Northern Hemisphere is currently experiencing large summer epidemics driven the spread of evolved BA.5 viruses. 1/11 https://t.co/P6bQ6DZhcF
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@trvrb Having 50%+ of the population catch covid every year with a IFR of 0.05% translates into an annual death count that we should not accept. We need to get transmission under control. We need to fund the development of vaccines that stop transmission, indoor air regulations &
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However, I doubt that IFR continues to drop that much further than 0.05%. And due to waning immunity and antigenic evolution of the virus we can expect continued widespread circulation with per-year attack rates of perhaps 50% or more. 4/5
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This level of circulation and severe outcomes (including long COVID in addition to death) combine to make "endemic" COVID-19 a serious ongoing health burden. Here, @dwallacewells describes this viscerally as "looking pretty brutal". 5/5 https://t.co/kmiWWJnH5I
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You can see this reduction in mortality rate in looking at projections of deaths from lagged-cases keyed to early case fatality rate. 3/5 https://t.co/0NtK1wIOMV
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Given vaccination and infection, the US and global population now has widespread immunity to SARS-CoV-2 and deaths per-infection are about 10 times lower than they were pre-immunity in 2020 with a ballpark IFR of 0.05% (though this will vary by immunity and age demographics). 2/5
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There seems to be a worry that telling people we've exited the "pandemic phase" will lead to further reduced precautions. As always however, I think it's best not to conduct messaging for intended behavioral effect and just try to make scientifically accurate statements. 1/5
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It turns out this average level of infection is equal to: I* = (1-1/R0)/(1+d_immunity/d_inf), where R0 is the reproduction number if everyone were susceptible. If we assume people are infectious for about a week, we get the following picture: 5/ https://t.co/y8wouGrGlb
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As variants accumulate, it can be tricky to track combinations of past exposures (e.g. https://t.co/AZOKtVccbj), but to get some intuition, let's assume people simply get infected, build immunity, then gradually become susceptible to infection again (i.e. because variants). 2/ ht
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