1/ The @nytimes has a good interactive story on the safety of flying during the pandemic, but they didn’t discuss boarding & deboarding. Judging by CO2 readings I saw on recent flights, this is the most dangerous part of flying. #covidco2#COVIDisairborne nytimes.com/interactive/20…
2/ By now there is overwhelming evidence #COVIDisAirborne. It’s transmitted mainly by shared air, i.e. inhaling the air others have exhaled, which contain aerosols—tiny, liquid particles that float suspended in air for seconds to hours, depending on size.
3/ There’s no easy way to measure virus levels in the air, but CO2 is a good proxy measure of risk. Outdoor CO2 levels are ~410 ppm, but since we exhale CO2, indoor concentrations are higher. The higher the CO2 level, the more air you’re sharing.
4/ I used an Aranet CO2 meter, which was tested & recommended by @jljcolorado, a top aerosol expert. I flew from Ft. Wayne, IN (FWA), to Rochester, MN (RST) with a layover at Chicago. FWA was not busy, & the CO2 ranged from 516 to 546 ppm.
5/ When we first sat down on the plane, the CO2 level was at 1424. Four minutes later, it was 1470. Over the course of the next 6 minutes, the CO2 concentration rose steadily.
6/ In the next four minutes, the CO2 level rose from 1654 ppm to 1899 to 2027 to 2255. Most IAQ experts, including @linseymarr, recommend keeping CO2 below 700 for a multitude of reasons.
7/ The next two pictures are quite blurry because the plane started to move, but you can tell the CO2 rose to 2343, then 2351 ppm.
8/ I think the ventilation system started bringing in outdoor air when the plane began taxiing but that it took a couple minutes for the CO2 to begin to decline. Two minutes after peaking at 2351 ppm, it had decreased to 2026, and two minutes after that it was 1738.
9/ By the time we took off the CO2 was around 1400 ppm, and it stayed right around that level for the entire flight.
10/ Chicago’s O’Hare Airport appeared to have quite good ventilation. The CO2 level stayed in the low-600 range where I was. I did not venture into the crowded cafeteria area nearby, where I imagine the levels were significantly higher.
11/ The next flight was to Rochester, MN, also on American Airlines. Immediately after boarding, the CO2 was already at 2096 ppm.
12/ Five minutes later, the CO2 concentration had risen to 2393 ppm, and in the next two minutes it rose further, to 2548 before peaking at 2650 ppm.
13/ At this point there was a revving noise, and CO2 levels started to decline, falling to 1820 ppm seven minutes later. 20 minutes after the peak 2650 reading, CO2 had declined to 1292 when we started taxiing.
14/ After taxiing for several minutes, we stopped. CO2 once again rose, but only to 1546, after which the plane started rolling again and levels declined.
15/ During this flight, which seemed equally crowded as the first flight and on a similarly small plane, CO2 concentrations were lower, ranging between 900-1030 ppm. Notably, relative humidity got as low as 12% later on in the flight.
16/ The Rochester Airport wasn’t very crowded, but with CO2 at 492 ppm, it still must have had good ventilation. Doors about 10 meters away likely helped.
17/ I’ll stop there for now. Later I’ll add info about the CO2 levels at Mayo Clinic and our hotel. Our return flights, again with a layover at O’Hare, are later today, and it will be interesting to see how they compare.
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@SolidEvidence There was yet another paper this week describing someone chronically infected, with serious symptoms, but who repeatedly tested negative for everything with nasopharyngeal swabs. On bronchoalveolar lavage (BAL), they were Covid-positive. 1/ ijidonline.com/article/S1201-…
@SolidEvidence BAL is very rarely performed, yet there must be dozens of documented cases now where NP-swab PRC-negative patients who were very ill tested positive by BAL. This has to be way more common than we realize.
If we had a similar GI test, I imagine we'd find something similar. 2/
@SolidEvidence Importantly, the patient was treated and improved, likely clearing the virus for good. Many, maybe most, chronic infections could be treated and cleared. But they have to know they're infected for that to happen. 3/
Read full 🧵for explanation, but the short story is that the best apparent escape mutations all interact w/something else—like a nearby spike protomer or other important AA—making mutations there prohibitively costly.
In short, the virus has mutated itself into a corner. 2/6
It's very hard to effectively mutate out such a local fitness peak via stepwise mutation in circulation since multiple simultaneous muts might be required to reach a higher fitness peak. 3/6
It's an interesting thought. I think the evidence is strong that all new, divergent variants have derived from chronic infections. The first wave of such variants—Alpha, Beta, Gamma—IMO involved chronic infections lasting probably ~5-7 months. It's controversial to say.... 1/15
…that Delta originated in a chronic infection, but I think the evidence that it did is strong. One characteristic of chronic-infection branches is a high rate of non-synonymous nucleotide (nuc) substitutions (subs)—i.e. ones that result in an amino acid (AA) change. 2/15
For example, if 80% of nuc subs in coding regions cause an AA change, that’s a very high nonsynonymous rate. The branch leading to Delta has 17 AA changes—from just *15* nuc subs! That’s over 100%. How is this possible? 3/15
I'd add that XEC's had no noticeable impact on cases & isn't likely to going forward barring a serious change, which we've not seen since S:Q493E & the glycan-adding S:S31-/S:T22N appeared months ago. Next major change seems likely to take the form of an entirely new variant. 1/4
I've been in lockstep with @SolidEvidence and @JPWeiland on this front. Despite the sensational early growth advantages XEC appeared to have, it never seemed likely to me ever to have a noticeable real-world impact. 2/4
In fact, XEC resembles BA.5.2 + ORF1b:T1050N, which had a similar growth advantage in summer 2022. That one, however, never had a sexy name like "XEC" that was distinct from other major contemporary variants so it passed unnoticed. Names matter. 3/4
Molnupiravir-created mutants still show up intermittently, mostly in Australia and Japan. A remarkable one popped up today: A KP.3.1.1 with 94 private mutations. 1/6
The closest related sequences are from the same region and from about 1 month earlier, suggesting these 94 consensus mutations were acquired in about one month, and possibly a shorter period of time. 2/6
It has the classic MOV signature of an extremely high percentage of transversions, primarily C->T and (especially) G->A.
93/94 mutations are transitions
27/94 are C->T
38/94 are G->A
More detailed discussion of this in 2022 thread below.
There aren't many convergent mutations in ORF1b in chronic-infection sequences. But many of the ones that do show up repeatedly are also highlighted in this study looking at NSP12 mutations that developed in immunocompromised pts treated with remdesivir. 1/4
I've spent hundreds of hours compiling a list of >3500 likely chronic-infection sequences & have created an imperfect, approximate measure for how overrepresented a mutation is in chronic sequences compared to circulating sequences (as measured by independent acquisitions). 2/4
Of the top 10 ORF1b chronic-infection-specific mutations on this list (occurring ≥5 times), five appeared in the remdesivir-treated patients in this study: Q435K, C455Y, V783I, M785I, & C790Y.
V783I was in 2 study patients & is also the most common of these in chronics. 3/4