Ryan Hisner Profile picture
Apr 22, 2021 17 tweets 7 min read Read on X
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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More from @LongDesertTrain

Jun 10
Another fantastic preprint on BA.3.2's propensity for children, this time from @yunlong_cao & co.
They not only confirm the findings of David Ho's lab (that kids have ~0 antibody response to BA.3.2) but dig into the details of exactly why kids are so vulnerable to BA.3.2.

1/4
Two big wins for vaccination & mRNA vaccines:

1. Kids vaccinated before being infected have robust antibodies against BA.3.2

2. Unvaxed adults much more vulnerable to BA.3.2, esp. compared to mRNA-vaxed adults.

Read @yunlong_cao's 🧵 & very readable paper for details. 2/4 Image
There's still one major paradox here I can't wrap my head around: countries with the highest vaccination rates & the lowest proportion of children appear—very low sequencing makes hard conclusions difficult—to have the highest proportion of BA.3.2. 3/4
Read 6 tweets
Jun 4
New data from David Ho's lab showing that while adults & kids have ~equal antibody responses to XFG & NB.1.8.1, children have essentially no neutralizing antibodies to BA.3.2.

This seems to largely solve the BA.3.2 + kids mystery. 1/14 Image
If you've missed the story about how BA.3.2 (a novel, divergent saltation variant) is hugely overrepresented in sequences from children, this was my original (very quick) analysis, which subsequent data extended & confirmed. 2/
More details from this preprint. 50 is the limit of detection (i.e. zero). Nearly all kids under 7 had no detectable nAbs to BA.3.2, despite robust nAb titers against NB.1.8.1 & XFG.

Notably, most kids also had zero nAbs to ancestral D614G or XBB.1.5. 3/
biorxiv.org/content/10.648…Image
Read 14 tweets
Mar 26
So it's clear that BA.3.2 preferentially infects children, something we have never seen before in a SARS-CoV-2 variant.

Why?

The question's baffled me, but after a suggestion from Darren Martin, I think I have an explanation that makes sense.
1/16
I've tried to make sense of BA.3.2's penchant for kids by considering its unique spike: more compact, more closed, & more antibody-evasive than any other variant.

But I think another feature of BA.3.2 is responsible: its wholesale deletion of ORF7a, ORF7b, & ORF8 (∆ORF78).
2/
∆ORF78 is rare but not unheard of; it was in several late XBB variants (GW.5.1.1, FW.1.1, GE.1.2, etc) & a few branches of other variants. I've long thought these late XBB had an advantage in some population subsector, but I didn't suspect kids.
3/
Read 18 tweets
Mar 24
You have to wonder for how long we will continue seeing infections from 2020 continue to show up (in absurdly high quantities) in wastewater.
1/16
I suspect that the number of people continuously infected since 2020 or 2021 is much larger than we realize. It's impossible to prove, but there are case studies where a chronically infected person gets infected by a new variant, which drives out the original virus...
2/16
...which consequently leaves no trace that the person was chronically infected before the super-infecting variant—took over.

Why then are some Cryptic WW variants resistant to being outcompeted by newer variants?
3/16
Read 16 tweets
Mar 22
While the final outcome for BA.3.2 is uncertain, its unique characteristics—extensively remodeled spike NTD & SD1/SD2, novel S2 muts, & total deletion of ORF7a/7b/8—make it the best candidate for co-dominance we've seen, which could mark a new era in SARS-2 evolution. 1/
Until now, the broad pattern of SARS-2 evolution has been:

1) Emergence of a saltation variant originating in a chronic infection

2) Rapid growth/global dominance & a variant-driven wave of infection—especially if it emerges in late fall/winter (BA.1, XBB.1.5, JN.1). 2/
3) Stepwise evolution over the next few months/years, usually without driving major waves (the JN.1-descended KP.3.1.1 being a notable exception).

4) Repeat

3/
Read 34 tweets
Dec 29, 2025
Very proud to be a co-author on this comprehensive preprint on the novel, growing saltation lineage BA.3.2, together with @Tuliodna, Darren Martin, Dikeledi Kekana, and lead author @graemedor. 1/9
I would normally write a summary 🧵 of the BA.3.2 mutational analysis here, but as much of my contribution parallels my previous BA.3.2 threads I'll just link to those here, w/brief descriptions of each.

This is my first, big-picture BA.3.2 🧵. 2/9
Short thread from June when the first travel BA.3.2 sequences showed up. I think my prediction from back then has pretty much been borne out. 3/9
Read 9 tweets

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