Very provocative new paper by @dylanhmorris @jlloydsmith on effects of temp & humidity on survival of SARS-CoV-2 on surfaces. Need to be careful in interpreting most novel aspects of this paper.
Thread. https://twitter.com/dylanhmorris/status/1317452511624790017
Background
Effects of temperature & humidity on survival of viruses is potentially of huge importance as it can influence transmission b/w people & has been argued to be key mechanism driving flu seasonality. See perspective by @mlipsitch C Viboud https://www.pnas.org/content/106/10/3645
New paper suggests that viral survival on surfaces declines w/ temp & is lowest at intermediate humidity. If robust, could guide how to reduce risk of indoor transmission - warmer & 40-60% RH best. Indoor risk v important for next 4-6 mo. But...
I have some concerns w/ this interpretation for several reasons:
1) data/analyses in paper itself: estimates of viral half-life are estimates from regressions (sometimes extrapolations) of estimates of raw data & N=3 w/ 10x variation among N=3 points.
Note: This work is challenging and requires BSL-3 lab. Credit to authors for studying infectious virus, not decay of RNA. But need to be careful in overstretching results, especially when data are limited & messy & results at odds w/ other results.
-Authors choose half-life as key response variable but this point is on edge of data for 8/9 treatments. Why not use time to decrease 90%?
-Slopes don't seem to go through data on key panel (10C 85% RH); slope looks steeper, residuals patterned?
-Another key panel (22C 85% RH) has no data for early time point so 1/2-life is extrapolation. Initial titres for other 85%RH are much higher (10C: ~10^3.5) or a little lower (27C: 10^2.5) than estimated intercept. Despite this CI extremely tight. Puzzling.
Why am I scrutinizing the high humidity treatment? B/c pattern proposed here - that viral survival is actually higher at higher humidities - is at odds with some data for other viruses. e.g. messy data from:
https://www.pnas.org/content/106/9/3243
This fig from paper supposedly brings in data from other viruses but I can't see pattern in it (can authors re-plot w/ 1/10th-life vs RH for diff temps?):
-Finally, experiment has just 3 humidities & is proposing a non-linear relationship. That's asking quite a bit from the data which, as noted above, are estimates of 1/2-lives based on regressions of N=3 estimates of TCID50 for each time step, temp, RH.
3) New study is on viral survival on surfaces. Epidemiological data indicate this is a relatively minor pathway in SARS-CoV-2 transmission. Anecdotes exist (including recent NZ trash lid) but just anecdotes so far.
https://twitter.com/DiseaseEcology/status/1279097818351726592 https://twitter.com/DiseaseEcology/status/1313193505276133376
How does relative humidity affect transmission via aerosols/droplets? Animal study (golden hamsters?) would be ideal for this. Does study already exist? If so, please link to it.
So, would I make policy based on this paper & try to have indoor buildings (e.g. schools) maintain humidities at intermediate levels (40-70%)? No, I don't think it's strong enough for that, especially w/ other transmission pathways & possible effects of RH on susceptibility.
In contrast, the patterns of Temperature here are strong and consistent with other results. Warmer air greatly reduces viral survival - compare 27C vs 22C.
So warmer air is much better than cooler air, and very dry air is bad. Meat packing, ice hockey - unfortunately good conditions for high viral survival (on surfaces).

But is very humid air also bad? I'm not convinced, but could be.
Addendum- flu data vs humidity above is transmission among lab animals not survival. Will add survival data tomorrow.
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