The Famulare family COVID saga continues. Up today: rebound 🤬 

https://x.com/famulare_mike/status/1895616959083053369

With my wife Marisa's consent, here is our estimated nose/throat viral load history relative to peak since I first tested positive on day 2 of my symptoms. We're both experiencing rebound!

Here's the same with log10-y. So yeah, we've both rebounded. I took paxlovid days 3-7 (and have been on metformin since day 2). My load crashed by day 7 and went negative days 9 and 10. Marisa hasn't had any treatments, and never went negative, but 10-fold rebound regardless.

BTW I described how to turn rapid test color into a quantitative assay here https://x.com/famulare_mike/status/1894899637217304636, and here's the code and data https://github.com/famulare/famulare.github.io/tree/master/assets/2025-02-26-My-First-COVID-Infection. 

First, it's annoying! We're very ready to be done. We're tired of not having Marisa's parents visit. Of masking around our toddler (who hasn't caught it yet, as far as tests and symptoms say). Of runny noses. Of being tired. And Marisa, who has had it worse, is tired of coughing!

But, because at least it's fascinating, I've been doing a lot of rapid tests on interesting samples on myself. So let's get into some interesting stuff. 

I tested on day 11 after testing negative twice because I noticed my nose was running just a little bit more and I was a bit more tired than the day before, and I was curious about rebound. Sure enough, I got a very faint positive.

That night, I was visited by GI distress! This is not a big surprise as we know COVID is shed in stool and can settle in the gut for the long haul, especially in someone like me who takes a B-cell-depleting therapy for MS and can't make new antibodies.

That said, I've tried three different approaches to get a fecal rapid test, but all have been negative. But I can't be sure if the virus isn't there or the tests don't work with that medium... 

- first try: sample probably too acidic: got weird transient positives on flu B and rsv but always covid-neg
- second: swab of solids, one minute in buffer, covid-negative
- third, swab of toilet water + solids, 5 minutes in buffer, covid-negative 

@SolidEvidence thoughts?

So anyway, stool sampling with rapid tests has been a letdown, but mask, hepa, nose, and throat sampling have been interesting! Here's a panel of days I tested samples from sites other than combined nose-throat. Y-axis is est. viral load relative to nose-throat day 2 (peak).

First up, masks. tl;dr: mask and nose viral load tell different stories over time! And I'm very likely a lot less infectious via the air now than at the start. 


As discussed here, on day 2, I was able to pull virus off a mask worn for an hour https://x.com/famulare_mike/status/1893095652462338263. In front of the mouth was highest viral load, with a very little but non-zero positive away from the mouth. (Wasn't negative like I originally said.)

Overnight from day 2 to day 3, I was able to pull virus off a mask put inside my bedside hepa filter, showing that SARS-CoV-2 was travelling on fine aerosols.  You see that quantified here, as the day 3 hepa measurement. https://x.com/famulare_mike/status/1893370704663568511

On day 8, my nose-throat viral load dropped by a factor of 1000, give or take, and my mask sample was negative, despite wearing it for 11 hours. So good, nose way down, aerosol negative.
https://x.com/famulare_mike/status/1895616959083053369

But, on day 12, my nose/throat sample is hot a hell again!  Dammit, how infectious am I???

I wore a clean mask for 4.25 hours, through work, talking, singning Moo Baa Fa La La to my daughter, etc. Tested the mask. It was barely positive--at the limit of detection but it's there.

But quantitatively, while my nose swab viral load on day 12 was about ~1/2 of the value on day 2 (so basically the same), the mask viral load is at least 500x lower! Overnight hepa was negative. This is great! There was very likely zero SARS-CoV-2 in my lungs last night. 

Even more interestingly, I tested nose and throat independently, instead of with a combined swab. Nose is strongly positive, almost exactly the same test-line-contrast-adjusted level as the nose-throad swab earlier that day. And the throat-only swab was negative.

Throat-only negative. Mask barely barely positive. Nose hot as hell. So? 

It's very likely I've got no infectious breath, no infectious spit, but very infectious snot. My only symptoms right now are fading GI, and one stuffy nostril. 

NOW I STILL BETTER KEEP WASHING MY HANDS 😂

So anyway, there's what I hope is a fascinating look into a single infection history, so far. I'm disappointed the stool tests are negative, but, as my symptoms calm down, I hope it's because there's very little virus there. I also really hope my wife and I clear this thing soon.

Until then, I'll let you know if anything else interesting comes up. Thanks for reading along!

You can read the unrolled version of this thread here: https://typefully.com/famulare_mike/by5EIud

The Famulare Family COVID Saga: A Rebound Story

Next thread: relative infectiousness via mask samples. tl;dr: I'm probably at least 5000x less contagious yesterday (day 8 of symptoms, day 5 of Paxlovid) than I was on day 2 (peak). 

https://x.com/famulare_mike/status/1894899637217304636

As I lazily described here, you can do some simple image processing to make rapid tests quantitative https://x.com/famulare_mike/status/1894899668787818579

And here I showed how to test an n-95 for exhaled virus https://x.com/famulare_mike/status/1893095706396946940

So we can put these together and compare exhaled viral load changes with nasal/throat swab changes, to get as close a proxy for contagiousness as possible!

Unfortunately, I only have two good mask samples (because I wasn't planning on doing this quantitative stuff until a few days ago). 

- 1 hour on day 2 of symptoms when I was red hot by nose

- 11 hours yesterday (day 8) when I was still faintly positive at ~200x lower viral load

The day 2 mask after an hour was positive, solidly at the mouth and juuuust barely at the top by the nose, out of the jet zone. (The side sample looks negative by eye, but the brightness dips very slightly, from background ~140/255 to test ~137/255, as seen with a color picker.)


The day 8 mask, even after 11 hours, was NEGATIVE negative. No signal from background at all.

So, just for fun, the figures below shows the precise estimate for the relative viral load for the nose and mask on day 8 vs day 2, and the upper bound for the mask


As you can see, quantitatively, I’m at least 5000x less contagious via the air than yesterday (and possibly infinitely less). So, I am very very likely no longer contagious! I’m also at least 70x less infectious by saliva. So I probably can't infect anyone else now!

I will mask until twice negative on the nose because why not? (Also, gotta watch for rebound!)

How cool is it to have quantitative measures of contagiousness?! With an app reader for the image processing, and instructions for mask testing, everyone could have this.

With more rigorous correlation of antigen test color, pcr ct, and existing studies correlated ct with transmission, we could have quantitative transmission risk measures for anyone who tests. Beyond satisfying my curiosity, I hope having these examples will help me advocate.

Addendum: I'm out of FlowFlex and iHealth tests, so I got a few crappy BinaxNow (I can't get a solid control line on these...), and I'm nose/thoat negative on Day 9.5. The upper bound is probably above my last two FlowFlex, so not sure what to make of it. 

Still tired and taking daily naps, but otherwise fine. Fingers crossed I throw a few more negatives and I'm freed on Monday. 

The Mrs is doing well too, but still testing quantitatively more positive than me. 

Daughter holding negative. Thanks masks, HEPAs, and windows!

My COVID: Infectiousness Variations via breath and nose

New COVID personal science thread: observations on viral load.🧵

Fun inside!

Viral load plummeted after 4 days of Paxlovid. I did some math* to estimate changes in viral load. 

*somewhere between back-of-the-envelope and semi-quantitative modeling
https://x.com/famulare_mike/status/1894124001204867424

As you can see, I went from screaming hot viral load on symptomatic days 2 thru 5, to very low but still detectable on day 7.  Along the way, on day 5, I lost much of my sense of taste and smell, but it started coming back yesterday and is not bad today. 

https://x.com/famulare_mike/status/1894155423659561000

Because I'm annoyed we don't have app readers to turn rapid tests into semiquantitative readouts of viral load, even though it's obvious to everyone who uses them that you can read out relative viral load with the intensity (and time to positive), I did some analysis.

First, convert to grayscale and use a color picker to grab approximate absolute brightness data for the test line, the control line, and the test strip background. Put that in a spreadsheet and plot. 

Second, normalize the test and control data by the background to get the excess darkness relative to the lighting and materials (and put it on a log scale). The control line is less variable now, although there is still a difference between flowflex (day 2,7) and iHealth.

So, we go one step further to normalize the test line darkness relative to the control. And now we have a nice time trend of antigen detected. 

And since the y-axis units don't have an absolute scale anymore, let's also just plot it as adjusted darkness relative to peak. What we see by eye at the top is now clear: after a small decline in antigen detected over the first 5 days, day 7 was ~12x less intense.

From there, what does that mean for my viral load (and likely infectiousness). For that, we need some idea of how more quantitative measures like pcr ct and genome copies vary with lateral flow test antigen binding. I couldn't find one paper that does that for either test, sooo

So I stitched together some bits from a few papers to get the gist. 

1) https://pmc.ncbi.nlm.nih.gov/articles/PMC11237673/pdf/spectrum.00073-24.pdf 
2) https://pmc.ncbi.nlm.nih.gov/articles/PMC9031584/
3) https://www.nature.com/articles/s41598-021-02128-y

I'm too tired right now to document for twitter how the next few images came to be, but I'll post code eventually..

A careful look at this stuff finds that genome copy number is not linear in antigen test line intensity. Rather, depending on the dataset and the paper, you can work through either direct genomes vs intensity or genomes to ct to intensity to find...

genome copies is proproptional to color intensity to a power of between-ish 1.4 and 3. I think what's going on is intensity is linearly proportional to genomes at low signal, but nonlinear diffusion-binding-optical junk kicks in at higher concentrations, so studies differ.

And the dynamic range of rapid tests with pcr ct is well-known to be something like ct =15 (for the hottest infection ever) to ct ~30 for rapid test negative. 
https://pmc.ncbi.nlm.nih.gov/articles/PMC9031584/

So anwyay, with that in mind, I can stich together estimates of the pcr-equvialent ct value I would've likely had, and the relative genome copies from peak. Here ya go!

This is cool, because I find it really useful to know that I'm something like 30-200x less infectious per minute of contact than I was a few days ago. 

At onset, I could've been an epic superspreader if I hung out in a crowded space. I felt fine. I've mostly felt fine this whole time. If I wasn't very curious (and thought I might have flu), I'd never have known! Even with so much immunization, superpreading remains a thing.

Second, now I still have to be cautious around my family, but I am able to feel a lot more relaxed about my n-95 getting the job done. That takes a large mental load off. 

Anyway, I wish we had standard tools for this. This kind of thinking would be way easier if it was just published for every test. And, I didn't do this analysis for mask viral load (aerosols), but nose/throat swab. It would be easy to make that correlation standard too.

We could know so much more about bespoke, personalized infectiousness! Which would make mitigation easier, more specific, and more palatable. I was hoping that future would come to pass 4 years ago. I hope for it still!

You can read the unrolled version of this thread here: https://typefully.com/famulare_mike/M7r3MoL

Observations on Viral Load and Recovery

Round 2: it’s airborne! 🧵

https://x.com/famulare_mike/status/1893095652462338263

Last night, I put a mask filter inside my hepa and left it near my pillow, in the direction I tend to face while sleeping, about 18 inches away. Because the mask was inside the machine, there was no path for ballistic droplets to get to it. Only exposure is fine aerosols.

Why near the pillow? Because I also ran the fan blowing out to keep viral concentrations low and to prevent leakage into the house. CO2 ~525ppm all night.

Result after testing a square centimeter of mask filter? Positive! (Nose/throat this morning on left, overnight HEPA on right). 

Despite only covering ~1/4 the hepa filter surface with a mask, and being in a very well ventilated room, I got direct evidence of virus excretion on fine aerosols.

Not a surprise as it’s been very well studied, but fun to see at home! There really is no room left for doubt.

You can read the unrolled version of this thread here: https://typefully.com/famulare_mike/79Yx21G

Thankfully still feeling fine. Started paxlovid this morning, so the next round of experiments will be about how fast viral load crashes out. Stay tuned!

SARS-CoV-2 is airborne: home edition

Feeling okay so far, so let the science fun begin!

(Not gonna lie, I've been happy to avoid COVID for the last 5 years, but I've been looking forward to having fun with it, god-willing, when it got me.)
https://x.com/famulare_mike/status/1893061064662884675

First, this red hot positive today is on what I think is day 2 of symptoms. 

Interestingly, my first symptoms were probably achey legs yesterday. (Vascular disease much??) Since last night, mild sore throat and some stuffiness. Was expecting flu or nada, COVID was a surprise!

Now, to the fun. I put a fresh 3M Vflex n-95 on for the last hour. And then I cut two pieces out. One from right in front of the mouth/nose, and one from the top side as far from the droplet "splash zone" as possible. And then put both cutouts in rapid tests. Result?

The line-of-fire center sample was positive after about a minute, and maybe doubled in intensity over the remaining 14 minutes. I have no cough or sneezing at all, and so this is a measure of virus excreted during tidal breathing.

The side sample from top-left of the nose was negative. 

Each sample was about 1 cm^2 in area, from a total x-sectional mask area of ~200 cm^2. With the mask on, the side surface is nearly parallel with the breath jet, and is far off-axis. So the effective x-section is very low.

While this is far from a careful test, it's interesting to notice that perhaps the quality of the seal isn't that important for source control, provided the jet region is well-covered. Something to perhaps find some comfort in if when worrying about fit factors on "baggy blues".

This can't disambiguate droplet from fine aerosol shedding. I'll put a mask cutout over the filter material in my HEPA overnight to see what happens. But I also have a box fan blowing out for negative pressure, so I'm not sure there will be enough buildup to measure.🤞🏻 we'll see!

You can read the unrolled version of this thread here: https://typefully.com/famulare_mike/iok2rPO

My COVID Surprise: fun science

After a lovely yesterday of festivities with three generations of chosen family, my wife’s gift to me is time to do whatever I want. Adrift after a sweet morning of tv and cuddles, and waiting to get the courage for a bracing swim, I find myself needing to write about my dad 🧵

My dad has never asked to come visit his granddaughter. Since my first trip to Seattle nearly 20 years ago, where he came to help me move, he’s never asked to come visit me. He hasn’t texted today, and it’s late enough to know he won’t. And yet, I still miss him.

My dad, George Edward Famulare Jr, is a 9/11 survivor. Before becoming a survivor, he helped organize an evacuation. After, he helped reconnect lower Manhattan with the world. https://www.nytimes.com/2003/01/06/nyregion/sturdy-survivor-gets-back-work-herculean-effort-restore-landmark-battered-9-11.html

Turns out we’re cut from the same cloth. I also jumped into action when a disaster landed on my working desk in January 2020. https://www.seattletimes.com/seattle-news/how-big-will-the-coronavirus-outbreak-get-this-bellevue-scientist-is-figuring-that-out/ And I know people are alive today because of it. And I will always be proud of that.

But we’ve never talked about this shared bond. After 9/11, he withdrew into a frenzy of work. Throwing all his trauma into saving a building. Giving all his energy for human connection to another survivor, with whom he since has another son who to this day does not know I exist.

I too threw myself into work. Amplified trauma on trauma, for far longer than I can say saved lives, or at least far beyond when I was among the unique group whom History gave no choice, and well after I could’ve metaphorically come back home.

After 9/11, I had empathy for my dad but I thought I’d do better than he did in his shoes. I was wrong. I’ve been a deeply flawed husband. Present in body but much too rarely in heart or soul. 

My wife has held out hope beyond hope, despite herself, that I will metaphorically come home. I’ve tried so many times. I am ever closer. But yet, like my father, my family still feels the pain of me choosing my hurt over them.

My dad will never come home. In that way, we are different. Because I will come home. I can only pray they are still there when I do.

But as long as I wait for him to come home to me—as long as I wait for him to call and say “I love you son and I’m sorry” and “I want to come out and meet Rosie”—I’m still stuck waiting for love that will never come, and my wife and daughter will wait for mine.

So goodbye, Dad. I’m blocking your number. I hope you see this, somehow.

Fuck you. I love you. I’m grateful for the lessons you taught me and the love you once showed me. But I was right—always right since I was a child—that I am stronger than you. I am going for a cold swim and then I am going the fuck home. Goodbye.

Goodbye Dad

Great to see estimates of the prevalence of chronic SARS2 from scientists working with the remarkable UK @ONS Covid infection Survey. Chronic prevalence (>60 days) was at least 0.1-0.5% in people infected before July 2022 (thru BA.1/2).

Gonna use this moment to grind an axe...🧵

https://twitter.com/Mahan_Ghafari/status/1760338169864618124

The interesting and frustrating thing is it was possible to guess this 2 years ago. How?

1) take patient self-reported symptoms seriously @ahandvanish https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8280690/

2) take the ONS long-covid symptom survey seriously (the best survey in the world for this).

Here's three slides I made in June 2022 stitching it together.

The first gives my biological interpretation of the symptom clusters.
1: looks like long tail of normal infection
2: looks like organ damage after acute infection
3: looks like new-onset autoimmunity or ME/CFS


the second slide (repeated here) maps that onto the ONS results for post-covid onset symptoms lasting 12 or more weeks.

The data on symptom correlations isn't available, but one can eyeball that cluster 1 ("looks like persistent infection") is about 0.1-0.5%.

We also get estimates of the long-covid prevalence in cluster 2 ("looks like organ damage") of 0.5-1.5% and cluster 3 ("looks like autoimmunity and ME/CFS") of 0.25-0.75%.  To my knowledge, these numbers, derived with the back of envelope in 2022, haven't been reported elsewhere.

The similarity between long covid that looks like chronic infection and observed chronic infection is striking.

It's actually a bit too striking. As the new ONS data reports that only 5-10% of the confirmed chronic infected have LC. Why am I still excited?

The authors of the new work are clear it's a lower bound. It's based on needed CT<=30 for sequencing (which isn't common at the tail of infections) from a nasal swab (which ignores other reservoirs, especially including the gut).

And in the opposite direction, the ONS symptom survey doesn't have a control group, and so the percent estimates are likely upper bounds for self-reported long covid symptoms due to long covid. (I know I'm poking a bear here, but *taps sign*).

https://twitter.com/famulare_mike/status/1689804196214943745

Albeit self-reported LC likely under-estimates LC because of social desirability bias to not be sick and lack of knowledge that the condition could exist.

Taken together, the sequence-based and crude LC survey-based estimates of LC prevalence due to chronic infection are, as reported, within a factor of ten, and the biases in both point to the middle. So I think they are roughly consistent.

This is great! Here's a picture of three different long covid syndromes and their prevalence (at least among those infected through mid-2022).
LC that looks like
- chronic infection of 0.1-0.5% of all infected
- organ damage of 0.5-1.5%
- autoimmunity and ME/CFS of 0.25-0.75%.

So why did I say I had an axe to grind at the top? I sat on these estimates for nearly 2 years, only showing them to some folks internal to BMGF. Why? Because there is no good venue to publicly share reasoned back-of-the envelope estimates in biomedical science.

Twitter doesn't work for this anymore. If this thread gets more than 20 likes, I'll be surprised.

The effort to go from some basic reasoning to a journal article is enormous. And I don't have the primary data anyway, so there isn't any real pathway to doing it even if it was worthwhile.

Anything resembling the blogosphere of 2008 is completely atomized.

Can we please have a journal of reasonable speculation? A place for clear thinking that can help move mental models in a field forward?

This isn't the most careful analysis, and I never intended it to be. But two years later, I still see people arguing about the one cause of long covid when it's multiple syndromes! I still see trials designed to test one mechanism of intervention when its multiple syndromes!

I still see insane estimates of long covid prevalence drawn from carelessly mining EMRs--things that do not fit naked eye observations of the fraction of newly disabled people in the workplaces, IRL friends and family, and schools of the people publishing the papers.

We need to do better. And it's not just that we need "better quantitative science." We need better reasoning about the world in biomedical science. And we need a venue to share better reasoning.

End of my rant. Now your turn to pile on!

Prevalence of Chronic SARS2: Insights and Frustrations

I started looking at COVID forecasting papers and got angry. To move on with my life, posting a few things.

tl;dr: a huge amount of effort was wasted on COVID forecasting, and the allure of forecasting without exponentially better data is continuing to waste a lot of effort.

Evaluation of ... forecasts of COVID-19 mortality in the US https://www.pnas.org/doi/10.1073/pnas.2113561119
Evaluation of the US COVID-19 Scenario Modeling Hub... https://www.nature.com/articles/s41467-023-42680-x
Predictive performance of multi-model ensemble forecasts of COVID-19 across Europe... https://elifesciences.org/articles/81916#content

In the US and Europe, the best models (typically an ensemble) all just barely beat "tomorrow is the same as today" on average for a few weeks.

But it's much worse than that.

From the eLife discussion:

"Across all models we observed that forecasting changes in trend in real time was particularly challenging... Our study period included multiple fundamental changes in viral-, individual-, and population-level factors driving the transmission of COVID.

"We observed a contrast between a more stable performance of forecasting deaths further into the future compared to forecasts of cases. .... We can link this to the specific epidemic dynamics in this study.

"First, COVID-19 has a typical serial interval of less than a week. This implies that case forecasts of more than 2 weeks only remain valid if rates of both transmission and detection remain stable over the entire forecast horizon. In contrast, we saw rapid changes...

Etc etc.

All three papers mention this, but above was the clearest discussion.

The forecast models fail whenever something about the system changes.

Trivial right? But those are the only times someone might actually need a forecast model!

The models work better than baseline when you could take a pencil and draw what's coming. As soon as you might actually need math and science, they immediately fail. Why? Because if you aren't forecasting what is changing inside the system, it's impossible to get anything right

for more than a generation time (or two, insofar as you won't notice how bad you're getting yet). Why a generation time? Because those outcomes are already determined--those people are already infected, so your transmission model doesn't matter at all.

Between the US and Europe, approximately 140 modeling groups participated in this forecasting nonsense. An absolutely outrageous waste of scientific effort. Scientists' lives. Grad students led away from expanding human knowledge. Tenured jobs filled for decades to come.

And forecasting remains a flagship focus of the epi modeling field. Conferences are full of presentations on a few percent improvement on proper scoring rules, with little or no discussion of absolute error and decisionmaking. Y'know, how forecasting might matter. It's BANANAS.

You can read the unrolled version of this thread here: https://typefully.com/famulare_mike/XQG49xe

My Frustration with COVID Forecasting

As an interested amateur looking to learn about personal far UV-C as an infection prevention tool, I did some playing with the 222nm irradiance data from the UV Can Lily from @joeyfox85. For those interested in learning along with me, here are notes:  https://twitter.com/joeyfox85/status/1575882717107224576

Caveat #1. Did I mention I'm an amateur? While I have earned my place to claim a fair amount infectious disease transmission expertise, when it comes to UV sterilization, I'm currently at the "white guy with a physics degree" stage of personal development. HERE BE DRAGONS.

Caveat #2. @joeyfox85 has nothing to do with me eyeballing a piece of paper he took notes on and then running away with it. Anything dumb is 100% on me, and I'm very grateful he shared the image for people like me.

If you're still with me, knowing that I'm an amateur trying out some open learning with a few folks I've recently crossed paths with on Twitter, read on.

Everything in this thread is supported with a script and the comments within here: https://github.com/famulare/far-UVC-exploration. Eyeballed data, a simple model of the irradiance field, and code to make some plots is here https://github.com/famulare/far-UVC-exploration/blob/main/uv_can_lily_CRUDE_SKETCH.R.

Here's the Lily. https://uv-can.com/products/lily-handheld-personal-far-uv-disinfection-light.

First thing that became really obvious is the simplest model of the light field, 1/r^2 decay from a point source, is quite wrong near the device. The axial intensity closely follows the geometry expected for the electric field of a disk with finite radius. https://www.physics.udel.edu/~watson/phys208/exercises/kevan/efield1.html

This decay is only linear out to an effective disk radius I find to be ~6.2 cm. This parameter must be a function of the reflector + lamp geometry, but I haven't tried to work out how. 1/r^2 doesn't fully kick in until >~ 20 cm axially away from the device.

Other good news is the fitted irradiance at the device face was 506 mu-W/cm^2 (and the residual around there is ~ +-15 mu-W/cm^2), which matches the manufacturer's stated value of of 490+ mu-W/cm^2. Good on UV Can for accurate specs.

Off-axis, the irradiance field >=10 cm out fits decently to the same distance dependence and falls off like cos(angle). Near the device, where there are no measurements in the tweet, we don't really know, but I can interpolate between observations and the surface intensity.

All together, we get a curve fitting model inspired by some some very basic physics for the irradiance field @joeyfox85 measured. It looks like this https://github.com/famulare/far-UVC-exploration/blob/f0df6fcd1125a4e7ec2f4a6dd582a6ade9a6510b/uv_can_lily_CRUDE_SKETCH.R#L108, with color is log10(irradiance) (cutoff at <1) and contours at 3,10,30,100. Looks okay! Residuals too!

(Well, the residuals are worse near the device, where the disk model is wrongest, but all are relatively small. There must be fat old books with formulae for incoherent beam cones, but I'm missing the right language and so I couldn't find them. If you have pointers, let me know.)

With the irradiance field, we can estimate that exposure time field for various amounts of viral killing. Figs below are based on https://pubmed.ncbi.nlm.nih.gov/35458414/, where they find one e-folding (68% reduction) takes 1/12.4*1000 = 80 mu-J/cm^2, and 10-fold reduction 80*2.3 = 180 mu-J/cm^2.

Note that this is a low required dose estimate compared to earlier work and for 254 nm light (https://iuva.org/resources/covid-19/Far%20UV-C%20Radiation-%20Current%20State-of%20Knowledge.pdf), but I'm using it because the Welch et al data is the most convincing to me and relevant IMO. Note also that it's a lot harder to get past 99% reductions.

Anyway, here are the estimated killing times for particles in the UV Can Lily irradiance field.

So what does this mean to me?

First is that the numbers in my old thread are too pessimistic, because the pure 1/r^2 assumption isn't right. https://twitter.com/famulare_mike/status/1573514122075181056  I think it's no longer obvious to me that personal devices at this power rating or a bit above can't work.

Second, irradiance fields alone do not answer the question of does personal UV-C work. Virus doesn't park itself and wait to die. What matters is the dwell time of virus in the vicinity of the light source, integrated over the irradiance field, before that air gets in your face.

All that physics and biology is a lot more complicated than can be grokked solely from a light field (at the irradiance levels considered). Two great reviews: https://www.cambridge.org/core/journals/journal-of-fluid-mechanics/article/effects-of-ventilation-on-the-indoor-spread-of-covid19/CF272DAD7C27DC44F6A9393B0519CAE3 and https://www.science.org/doi/10.1126/science.abd9149.

Effectiveness will vary widely, depending on how air mixes in and into the space between the incoming air, the light, and your face. I really want to see good physics-based modeling from people selling these devices, and I'm disappointed it doesn't seem to be available yet.

Third, all that having been said, the volume of a typical breath is ~0.5 L = 500 cm^3 = a cube ~8 cm on a side, and inhalation takes a few seconds. So if I have a Lily hanging under my chin and aimed at my nose, I expect it can kill about half of the virus about to enter my face.

That's not gonna help if the person sitting across from me is spraying me down, but, for transmission from the ambient air, transmission rates are linear in viral concentration. And so a 50% cut would be nice when a mask isn't an option! And more power--safely!--would be better.

Fourth, UV safety is also a major concern. I want to see much more clarity from device sellers, and eventual regulation, as consumers like me cannot easily verify safety. https://twitter.com/joeyfox85/status/1575882726225301504 Leaky lights can cause harm. (interesting paper: https://www.scienceopen.com/document_file/87fb0538-10bb-4e5d-9225-9f6844d83c1f/PubMedCentral/87fb0538-10bb-4e5d-9225-9f6844d83c1f.pdf)

Fifth, I cannot imagine any circumstances where a personal UV-C of this power is reliably as effective as a well-fitting N-95-equivalent or better. The wonderful thing about a good mask is it always does the same thing. Most external conditions don't change the risk reduction.

But we can't always mask or don't always want to. And so as part of a layered strategy for harm reduction, I remain interested in the role of far UV-C in general and personal UV-C in particular.  Let me know what you think, as we take this learning journey together.

You can read the unrolled version of this thread here: https://typefully.com/famulare_mike/DbPnT3k

Very amateur notes on the UV Can Lily personal far UV-C device

MFW all the hot takes on SARS2, polio, transmission blocking, mucosal immunity, and community-level risk differences collide🤯

The story of polio epi today is the story of how mucosal vaccines and clean indoor air will together be transformative against respiratory infections.🧵

Here's the shortest version I can muster... (42 tweets is not short.)

The ability of polio to transmit depends most strongly on contact network density, water and sewer sanitation, and immunity against infection (both mucosal and systemic). I will thread all these together below and point the way toward a much better future for SARS2, flu, etc.

Contact network density has the same effects on polio as for any communicable disease. More contacts = more transmission. But because the transmission routes are fecal-oral and oral-oral, it's mostly intimate friend and family contacts that matter except where sanitation is poor.

(Respiratory transmission was debated heavily back in the day, but was determined insignificant because poliovirus is only rarely found in lungs and nasal mucosa (early ref https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2135158/pdf/771.pdf). The dismissal of the airborne route is grounded in biology and not sloppy epi.)

So, poliovirus transmission rates depend on social context, but transient superspreading through indoor air is unlikely to be a big factor. Rather, the first big factor is water and sewer sanitation.

The story of polio and sanitation is rich and fascinating. If you read one article, choose this: From Emergence to Eradication: The Epidemiology of Poliomyelitis Deconstructed https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2991634/

In towns and cities without closed sewer and water systems, polio is at least as infectious as measles. Historically, almost everyone got the multiple strains very young, when protected from paralysis by maternal antibodies, and so "infantile paralysis" was sporadic and rare.

As sanitation improved throughout the late 19th and 20th centuries in much of the world, polio became an epidemic disease because people started getting it when they were older and no longer had maternally-acquired protection. Vaccination interrupts this in ways discussed below.

But, as sanitation improves even further, to reach standards most who live in high and middle income countries take for granted today, sanitation interacts with vaccination to become a friend again. (Immodestly) if you read one, choose: https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.2002468

Sanitation determines the typical fecal-oral exposure--how much poop you eat--under different living conditions. Everyone eats some poop everyday, but we infer that typical amounts vary by at least 4 orders of magnitude. 

So in some places, polio transmits through food, dirty water, latrines, touches, all sorts of different surfaces and fomites, (maybe flies) and... In other places, it only likely transmits via direct contact with oral secretions or something that has been in someone's mouth. 

This brings us to the role of vaccination and infection-blocking immunity. Why? Polio immunity is multifaceted and the effectiveness of vaccination against transmission depends strongly on sanitation!

There are two immunologically-relevant "compartments". Enteric mucosal immunity that prevents infections in the gut (primary site of polio infection) and systemic humoral immunity that prevents proliferation of poliovirus from the gut to other parts of the body. 

IPV, the Salk vaccine, when given to someone who's never had a live poliovirus infection, provokes excellent humoral immunity but almost-zero enteric immunity. So IPV rocks against paralysis (can't get to neurons) AND oral shedding, but not infection or fecal shedding.

So if you live somewhere with reliable water and sewer sanitation and where hand, food, and toilet hygiene standards are high, IPV alone will prevent both paralysis and transmission. This applies to most people in high and middle income countries. 

But, IPV alone doesn't do anything to prevent infection in the gut, and so it does nothing to prevent fecal-oral transmission. Thus, people who live in places without effective sewage and water sanitation infrastructure, or less hygienic practices, polio will still transmit.

Here enters OPV, the Sabin vaccine. OPV is a live-attenuated vaccine that is very similar to a wild poliovirus except it is 1-10 thousand times less likely to cause paralysis (depending on the strain). This replicates in the gut and provokes strong mucosal and humoral immunity. 

So OPV vaccination can shut down transmission in places without good sanitation. Hence its use in eradication, both historically in countries like the US that can now maintain elimination with IPV alone but couldn't do so 60 years ago, and in places where polio remains today.

(The catches with OPV are it doesn't cause zero paralysis and it's not different enough from wild poliovirus when it comes to transmission. That's also a fascinating and difficult story, worked through in detail here (again) https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.2002468, but not this thread's story.)

In summary, the epi of polio today is one where it does or can transmit only in communities that have the wrong combinations of under-vaccinated, insufficient vaccine effectiveness for their sanitary conditions and contact networks, and/or insufficient sanitation and hygiene.

Back to the top, I wanna highlight two lessons of polio for SARS2, flu, etc. The effectiveness of infection-blocking immunity depends on exposure. Large changes in exposure can lead to different transmission dynamics. Together, the epi can change drastically.

First, effective mucosal vaccines, if we can get ones that work in humans, will be great for reducing transmission. I feel like an optimistic but maybe realistic dream would be 80% effectiveness against infection that lasts for a year against all known circulating variants.

80% effectiveness turns R0=10 into Re=2, which would probably lead to SARS2 settling down into an influenza-like annual incidence. That sucks less than not having mucosal vaccines https://twitter.com/trvrb/status/1549847175172984832, but with long COVID at appreciable rates across all ages, it still sucks.

Similarly, there is a dose-response relationship to SARS2 transmission. https://elifesciences.org/articles/63537 With realistic indoor air interventions using current technology, we can pretty easily imagine reducing viral loads in the air also by a factor of 5 or so in lots of spaces.

Realistic indoor air interventions applied at scale would turn R0=10ish to Re=2ish, which is much better than where we are today (for ex, it would eliminate flu and rsv -- much better than vaccines alone), but still kinda sucks, because long COVID and an IFR still worse than flu.

I mean sure, these both look a lot more like influenza (but lurking long covid) and everyone this entire pandemic has framed a good outcome with SARS2 to be turning it into influenza, so that's pretty good right? But imagine combining mucosal vaccines and clean indoor air!

Combine 5x reduction in airborne viral load with a 5x reduction from mucosal vaccines and R0=10ish turns into Re=0.4ish. That's a pathogen that only circulates when either vaccination isn't happening or your clean air infrastructure fails. JUST LIKE WHAT HAPPENED TO POLIO. 

Clean air and mucosal vaccines working together is also more tolerant to the transient failure of either one. Say a new variant pops up and infection-blocking immunity goes to zero. We still have Re=2ish and very low prevalence. That gives more time to update vaccines. Better.

Or say mucosal vaccines don't work. We get infection-blocking from today's vaccines, but transient and variant-dependent. But w/ Re=2 from clean air, less vax efficacy is needed. With help from seasonality, both could annualize epidemics and make booster timing feasible. Better.

Or take spaces where we can't achieve a 5x cut in airborne virus. Those still have reduced R0. Many crowds cease to be superspreading environments. Restaurants and homes can be crowded with similar risks to flu, and transmission is still stopped in the clean air places. Better.

This is also the story of polio. Once you break the global transmission network, susceptible pockets can go years without infections. With the network broken, infrastructure and vaccination programs can wobble without massive epidemics. Just like with polio.

And as with polio, there will still be endemic reservoirs wherever we can't achieve the right combo of vaccine effectiveness and sanitation to bring R0 below 1. We will still have the problem of SARS2 anywhere is a threat everywhere--the fundamental challenge of global health.

But that's much better than the near future we're facing today. Indoor air quality infrastructure is essential, and mucosal vaccines will make a big difference, but the two combined will be transformative!

We're not used to thinking about this because we're not used to thinking about how vaccine effectiveness and environmental conditions interact. The polio literature is messier than the story I told because the synthesis that ties it all together is spread over a 150 years.

We're not used to thinking about the setting-dependence of respiratory vaccines because, without mechanical indoor air cleaning, the range of variation in sanitation across human societies is more like a factor of 10 than the factor of 10,000 or more for sewage and water.

But we should be thinking about sanitation and vaccines together.

Vax and sanitation together tells you why it's very unlikely that polio will explode in most of the world it's been absent from for years. Just as it explains why it's so hard to eradicate in places it persists, and why outbreaks happen where they do.

Vax and sanitation together tells you why some of us still imagine a world where endemic circulation of respiratory pathogens has gone the way of polio, and that it can be achieved with incremental improvements in existing tech, without "lockdowns" or masking forever.

But we have to stop being so damned insular and start learning from each other! And learning from the past. I hope maybe the afternoon spent writing this helps someone out there.

If you want to help me turn this into an article or a much shorter twitter thread, let me know! Tagging folks who may be interested. @VirusesImmunity @jljcolorado @linseymarr @EricTopol @ScottGottliebMD @florian_krammer @K_G_Andersen @HelenBranswell @mlipsitch @MarionKoopmans 

You can read the unrolled version of this thread here: https://typefully.com/famulare_mike/o7ZUHuD