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.

• • •

Missing some Tweet in this thread? You can try to force a refresh
 

Keep Current with Ryan Hisner

Ryan Hisner Profile picture

Stay in touch and get notified when new unrolls are available from this author!

Read all threads

This Thread may be Removed Anytime!

PDF

Twitter may remove this content at anytime! Save it as PDF for later use!

Try unrolling a thread yourself!

how to unroll video
  1. Follow @ThreadReaderApp to mention us!

  2. From a Twitter thread mention us with a keyword "unroll"
@threadreaderapp unroll

Practice here first or read more on our help page!

More from @LongDesertTrain

Jun 29
@suprion_verlag @dfocosi @yunlong_cao @RajlabN @BenjMurrell @SystemsVirology @SimonLoriereLab @EricTopol @TRyanGregory @tylernstarr @JPWeiland @siamosolocani @CorneliusRoemer The basic pattern has been that we occasionally see huge evolutionary jumps with no intermediate sequences (BA.1, BA.2, BA.5, BJ.1/XBB, BA.2.3.20, BA.2.86, & many others), which in reality evolved stepwise within a single, chronically infected individual.
@suprion_verlag @dfocosi @yunlong_cao @RajlabN @BenjMurrell @SystemsVirology @SimonLoriereLab @EricTopol @TRyanGregory @tylernstarr @JPWeiland @siamosolocani @CorneliusRoemer Then, after such a variant begins circulating, it begins to pick up mutations, primarily in the spike protein, which evade antibodies that are widespread in the population. The specific mutations vary somewhat with each new variant, but there's a lot of common ground as well...
@suprion_verlag @dfocosi @yunlong_cao @RajlabN @BenjMurrell @SystemsVirology @SimonLoriereLab @EricTopol @TRyanGregory @tylernstarr @JPWeiland @siamosolocani @CorneliusRoemer R346T, for example, has been acquired again and again. Various mutations at E484 and F486 have been common as well, and there are many others that could be mentioned. In some cases, these mutations seem to have arrived at a quasi-endpoint (for now)—∆Y144 or F486P, for example.
Read 5 tweets
Jun 18
. @BenjMurrell is doing the best variant growth modeling in the world, & his latest results confirm most of what we've thought: KP.3 is the fastest large variant, & its sublineage KP.3.1.1—w/the highly advantageous, glycan-creating S:∆S31—is easily the fastest in the world. 1/15
It can be a difficult to decipher the meaning of these graphs if you don't have an encyclopedic knowledge of the latest variants—which I think only @siamosolocani possesses—so I tried to add some context to Ben's graph, which I'll explain below. 2/15 Image
I divide key mutations into 4 categories, from most to least impactful, IMO.

#1. Q493E (KP.3 exclusive), F456L (~universal)
#2. T22N, ∆S31 (glycan-adding)
#3. R346T, T572I
#4. F59S/L, S60P, K182N, Q183H

Lowest row of boxes on the graph is group #1, above it #2, & so on. 3/15 Image
Read 16 tweets
May 8
KP.3 (w/the rare Q493E) has been my pick since I first noticed it emerging from numerous travel seqs from India. F456L & R346T are the typical stepwise immune-evasion mutations that, as @shay_fleishon noted, very likely impose a fitness cost. Q493E may be different. 1/
Q493E involves the rarest of all nucleotide mutations, C->G, and occurs at a key residue that we've seen very little action from of late. 493 mutations, however, are common in the Cryptics, usually Q493K I believe. (@SolidEvidence can correct me if I'm wrong on that). 2/8 Image
493 is also one of the few residues where mutations—on BA.1/BA.2 backgrounds—can confer large increases in ACE2 affinity—see @jbloom_lab data below. The 2-nuc Q493A & Q493V appeared in a handful of remarkable chronic-infection seqs, for example. 3/8 Image
Read 8 tweets
May 1
We have a new record for mutations in a non-molnupiravir sequence. It's a BA.2.12.1 with >100 private mutations. There are 4 seqs from early April, all from the same patient. I'll discuss four interesting features it has in this 🧵. 1/23 Image
#1) Reversions
Reversions are extremely rare. They almost never appear in circulating lineages. There are, however, a large number of reversions that are convergent in chronic-infection sequences. This one has more than usual. 2/23 Image
Let's start with my favorite.
• ORF1b:L314P (NSP12_L323P)
The extraordinarily rare yet hugely significant ORF1b:L314P reversion is an enigma. ORF1b:P314L was one of the very first SARS-CoV-2 mutations. It quickly dominated & has been universal ever since. 3/23
Read 23 tweets
Apr 19
What connects two regions on opposite ends of NSP12, a narrow slice of an obscure NSP3 region (DPUP/SUD-C), & a 3-AA sliver of nucleocapsid (N)? I have no idea, but I’m convinced there’s a link that could help reveal the inner workings of SARS-CoV-2. 1/120
Image
Image
I previously wrote a thread about the strange connection between ORF1a:4395-4398 and ORF1b:820-824 (NSP12_3-6 & NSP12_829-833). There is no known connection between these regions, & they are not close to each other in the NSP12 protein structure. 2/120
Mutations in both regions are rare, yet they arise in the same sequences again and again, at rates that cannot be coincidental. Furthermore, there have never been any circulating lineages with these paired mutations—they are a chronic-infection specialty. 3/120 Image
Read 124 tweets
Apr 13
Always nice to run across a possible function of a rare mutation that's shown up in multiple chronic-infection SARS-CoV-2 seqs. Thanks to an excellent paper by @TheMenacheryLab & @J_Paul_Taylor, I think I now know why N:L13P (a reversion) shows up. 1/6
They proved that the N:1-25 region, esp. the ITFG AA motif from N:15-18, is the essential element in N's ability to suppress the formation of stress granules (SGs) in cells, which capture & disable long viral RNAs & help organizing innate antiviral immune responses. 2/6
Image
Image
All variants retain the ability to suppress SGs, but Omicron's N:P13L weakens N's binding to G3BP1/2—the master cellular regulators of SGs—by about 2.3-fold. That's pretty slight, & almost certainly not enough selection pressure to result in reversions in circulation... 3/6 Image
Read 7 tweets

Did Thread Reader help you today?

Support us! We are indie developers!


This site is made by just two indie developers on a laptop doing marketing, support and development! Read more about the story.

Become a Premium Member ($3/month or $30/year) and get exclusive features!

Become Premium

Don't want to be a Premium member but still want to support us?

Make a small donation by buying us coffee ($5) or help with server cost ($10)

Donate via Paypal

Or Donate anonymously using crypto!

Ethereum

0xfe58350B80634f60Fa6Dc149a72b4DFbc17D341E copy

Bitcoin

3ATGMxNzCUFzxpMCHL5sWSt4DVtS8UqXpi copy

Thank you for your support!

Follow Us!

:(