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.
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 pnas.org/content/106/10…
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: pnas.org/content/106/9/…
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.
2) Suggestion that moderate humidity reduces viral survival needs to be weighed against impact of humidity on effects on lung tissue. Study @VirusesImmunity in mice indicates lower humidity increases susceptibility: pnas.org/content/116/22…
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.
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.
Adding link to thoughtful response (& my responses - it's a conversation) from @dylanhmorris:
My overall take:
Strong support for viral survival & transmission being highest at low temps, low RH.
Uncertainty about whether RH>50% increases or decreases risk
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How many SARS-CoV-2 infections are there per COVID-19 case now?
Early estimates & guesses suggested there were 10 infections for every case, but these estimates were done when testing capacity was very low. With higher testing capacity & better engagement where are we now?
Thread
Background
It's well known that confirmed COVID-19 cases are only a fraction of all infections. Infections can be missed because people are asymptomatic, have mild enough symptoms that they don't get tested, or can't get tested even if they want to due to accessibility.
In Mar-Apr underascertainment of infections was so large & uncertain it led to claims that there may have been hundreds of infections per confirmed case. A famous example is paper suggesting 1/2 of UK MAY have been infected by Mar ft.com/content/5ff646…medrxiv.org/content/10.110…
@CDCgov needs to harmonize/update all websites on spread of COVID-19
1 updated page has clear &(nearly) accurate information: cdc.gov/coronavirus/20…
(here's detailed thread on update:
)
Many other CDC pages still focus on wrong mechanisms of spread
Thread
Updated page is clear about #1 mechanism of spread:
close (<6') contact
It also makes it clear that further >6' spread is possible
("airborne transmission") & when this occurs (indoors, poor ventilation)
Perhaps most importantly it accurately tells people how to be safe.
Relative ranking isn't completely right, but pretty good (still too much focus on surfaces, hand washing). For far more details on update see:
How do we survive next 6-12 months?
Tweets by @TinaG_SD epitomize what many feel - even w/ relatively good measures in place, as in CA (mask mandate, bars/restaurants closed or nearly so, sick pay, etc.), transmission continues & cases ebb & flow & restrictions crush jobs.
Thread
These measures certainly help but don't seem to be enough (see previous tweet). Why?
Transmission of COVID-19 is inherently a 2 step process. Step 1: Transmission w/in households is rapid with whole households sometimes getting infected.
Step 2: Transmission between households.
CDC's updated webpage on how COVID-19 is spread & prevention tips is now (almost) in line with science!
(WHO please do the same!)
(Hooray! only 10 months into epidemic & when Trump in hospital so maybe isn't paying attention?)
Thread cdc.gov/coronavirus/20…
Webpage 1st summarizes dominant mode of transmission which is consistent with epidemiology data: mostly from people w/in 6' of each other & clearly states that people w/out symptoms (pre-symptomatic or asymptomatic) can transmit also!
2. Website give ranking of how easily SARS-CoV-2/COVID-19 spreads relative to flu and measles.
(I'm not sure this is supported by data. R0 is higher than flu, but might be due to length of infectious period, not higher infectiousness. Anyone know of data to support/refute?)
PSA: We (STILL) have no data to know the pattern of viral loads over time from infection to recovery. So we don't know how test sensitivity & infectiousness correlate.
Tons of stories w/ quotes from top people are not making this clear & it matters.
Clarifying thread
You may have seen this figures showing viral load over time, with thresholds for testing +.
(This one from @michaelmina_lab@DanLarremore paper). Simple & straightforward, right?
Conceptually yes, but what is this figure based on? Is it SARS-CoV-2/COVID-19 data in people? Nope!
This figure is (loosely) based on data from other viruses in people & SARS-CoV-2 in animals. Here's data from macaques (10.1126/science.abc4776) & cats (pnas.org/cgi/doi/10.107…). Looks similar to schematic but not quite identical. Where is the virus-negative period pre-peak?
I posted this thread earlier because there's a serious challenge ahead: now that antigen tests are being used on a huge scale (WHO bought 120M; Abbott is producing ~50M/month), key Q is: what to do w/ result?
CDC says: + antigen test = "presumptive case". wwwn.cdc.gov/nndss/conditio…
Understandably, this makes some health care professionals uncertain what to do next, especially if confirmatory PCR test takes days to get results back. Do they treat it like a confirmed case, try to get case to isolate & trace their contacts?
If few false +, no problem!
But if false +s are relatively common (even 1-2% would count as relatively common) & antigen tests are used for frequent screening of asymptomatic people, this would lead to large number of isolated/quarantined people, awaiting PCR tests. Here's an example...