How Colds Spread
It seems like a catastrophic civilizational failure that we don’t have confident common knowledge of how colds spread. There have been a number of studies conducted over the years, but most of those were testing secondary endpoints, like how long viruses would survive on surfaces, or how likely they were to be transmitted to people’s fingers after touching contaminated surfaces, etc.
However, a few of them involved rounding up some brave volunteers, deliberately infecting some of them, and then arranging matters so as to test various routes of transmission to uninfected volunteers.
My conclusions from reviewing these studies are:
You can definitely infect yourself if you take a sick person’s snot and rub it into your eyeballs or nostrils. This probably works even if you touched a surface that a sick person touched, rather than by handshake, at least for some surfaces. There’s some evidence that actual human infection is much less likely if the contaminated surface you touched is dry, but for most colds there’ll often be quite a lot of virus detectable on even dry contaminated surfaces for most of a day. I think you can probably infect yourself with fomites, but my guess is that it’s mostly aerosolized particles.
Small particle aerosol transmission[1] seems unlikely to transmit the tested cold viruses, but the meta-analysis is more equivocal than I am on that question.
Sitting directly across a table from an infected person, or otherwise having a face-to-face conversation with them, seems pretty risky. A separate “close-quarters” study suggests that likelihood of infection increased (approximately) logarithmically with hours of exposure, with a 50% likelihood at about 200 infected-person-hours of sharing space.
Fomites
This section may as well be called Gwaltney & Hendley, as they conducted basically all of the studies[2] suggesting that fomites might be a substantial vector of transmission.
Gwaltney et al., 1978 conducted three separate trials, each attempting to test a different method of transmission.
The large particle test[3] had 1 donor and 2-4 recipients sitting around a small table (0.7m diameter). Donors were instructed to talk loudly, sing, cough, and sneeze for the 15-minute period. Everyone wore rubber gloves while in the room. 1[4] out of 12 total recipients were infected.
The small particle test housed donors and recipients (1 or 2 recipients per donor − 6 donors & 10 recipients total) together for 3 successive days and nights in a large, closed room, separated by a double wire-mesh barrier to preclude direct contact. Everyone spent all their time in the common room except when in the adjoining bathrooms, or when the donors were being borrowed to expose other recipient groups in other arms of the experiment.
This resulted in zero infections! It seems like moderately strong evidence to me, and makes me update on small particle transmission being less likely; I don’t see obvious ways in which this test fails to replicate relevant real-world conditions.
In the fomite test, “donors deliberately contaminated their hands with nasal secretions as they would when blowing their nose”. Then they performed a 10-second handshaking procedure with recipients, both sides wearing surgical masks. Recipients then went to another room and self-inoculated by putting their fingers “on their nasal and conjunctival mucosa as they might under natural conditions”, two to three times (then washed their hands).
This infected 11 out of 15 recipients. Ok, if you go directly from a wet handshake to rubbing your eyes, you’re in trouble, noted. It’s not clear how this generalizes to more realistic[5] patterns of fomite transmission. Do people even shake hands nowadays?
Gwaltney & Hendley, 1982 directly tested fomite transmission via shared surface contact. This lets us screen off the risk of accidentally mistaking unintended aerosol transmission for fomite transmission. To summarize, they had donors blow and/or wipe their noses with their fingers, briefly handle a coffee cup or rub a plastic tile. They then gave those objects to the recipients to touch, and had the recipients put their fingers “in contact with the conjunctival and nasal mucosa” (i.e. rub their eyes or pick their nose).
Twenty minutes passed between donors contaminating the tiles and recipients touching them. (Ten minutes on each side of “either apply disinfectant, or not”.) The period of time between the contamination and then handling of the coffee cup handles wasn’t specified, sadly.
5 of 10 coffee cup recipients, 9 of 16 unsanitized plastic tile recipients, and 7 of 20 sanitized[6] plastic tile recipients became infected.
This seems like pretty strong evidence that indirect transmission via shared surface contact is possible. My prior on that was very high (especially given the previous study); it would be pretty surprising if it turned out that skin contact was load-bearing here. The self-inoculation procedure seems pretty similar, so we don’t get much evidence about how effective this route is under “more realistic” conditions.
I also looked at a couple “secondary metric” studies, just to check whether there was anything very surprising there.
Ansari et al. 1991 tested how much virus survived on both people’s fingers and metal disks, when directly applied. tl;dr:
Human parainfluenza virus 3 (HPIV-3): <1% of virus remained viable after 1 hour[7].
Human rhinovirus B14 (RV-14): 37.8% viable after 1 hour; ~16% still detectable after 3 hours
Maybe significant for HPIV-3, but rhinoviruses comprise most “common colds”, and those seem to stick around for a while.
Winther et al. 2007 tested two things:
What percentage of environmental sites sampled in hotel rooms occupied by cold sufferers were contaminated[8] with rhinovirus RNA (35%, and the types of things you’d expect—“door handles, pens, light switches, TV remote controls, faucets, and telephones”).
How likely fingertip rinses were to test positive for virus after touching deliberately-contaminated objects (not the same as the naturally-contaminated sites from the above), both 1 hour and 18 hours after contamination. “Rhinovirus was transferred from surfaces to fingertips in 18⁄30 (60%) trials 1 hr after contamination and in 10⁄30 (33%) of trials 18 hr (overnight) after contamination.”
The study didn’t test for the last leg, i.e. actual infectivity.
Aerosols
And this section, correspondingly, consists entirely of studies that include Elliot C. Dick as an author.
D’Alessio et al., 1984 ran 3 types of experiments with a total of 33 recipients. I’m really hesitant to draw conclusions from this one, because it had some surprising results that I think represent methodological issues.
The first experiment type had donors and recipients playing cards, talking, and singing together in a room for 2-3 hours. Across two rounds, there were 5 donors and 9 recipients. The researchers claim that none of the recipients were infected with RV55 (which they infected the donors with), but see this footnote to the data table for that experiment:
Three colds developed in recipients during the week after inoculation, but RV55 was not isolated from multiple nasal specimens, nor did antibody to RV55 appear in serum after the experiment. Three nasal specimens were obtained from each of the six asymptomatic recipients after exposure to RV55; tests of all of these specimens yielded negative results, as did serological tests.
So who knows, really.
The second experiment type had small groups of donors and recipients sharing dormitory rooms for 12 hours a day, 3 days in a row, and “to decrease the likelihood of transmission by fomites, participants were asked to avoid handling one another’s personal items and to use separate bathrooms”. There were 11 donors and 11 recipients, with 5 groups of 2 each, and 1 group of 1 each. The results from this experiment are reported as “one infection”, but once again:
Three recipients developed colds, but only one case of transmission of RV55 was confirmed by laboratory findings.
🤔
The third had donors kissing recipients: “Forty-eight hours after being infected with RV55, four donors kissed five recipients for 1 min. A second group of six donors, similarly infected, kissed 11 recipients for 1.5 min (two 45-sec contacts). Each recipient was kissed only once; the donors and recipients were instructed to use the kissing technique most natural for them.” They report only one instance of transmission here (recipient no. 16), with this caveat:
In four recipients (no. 1, 6, 8, and 12), cold-like symptoms developed during the week after exposure to RV55, but seroconversion did not occur and RV55 was not isolated from nasal specimens. A rhinovirus other than RV55 was isolated from recipient no. 8.
As I said above, the methodology here seems much less careful and the results are substantially sketchier; how likely is it that so many test subjects just happen to coincidentally catch a different cold after being exposed to one in the experimental setting?
Dick et al., 1987 had a very interesting, and substantially more robust, experimental design. The first stage, which they ran 3 times, was sticking 20 guys into a room with 4 tables. 8 of those guys had colds, 12 were healthy—each table took 2 infected and 3 uninfected guys. Half (6) of the uninfected guys wore restraining devices meant to prevent them from touching their faces. In the first of the 3 rounds, this device was a “large, clear plastic collar… worn around the neck and supported by the shoulders”.
In the second and third rounds, they wore arm restraints “composed of two halves of an orthopedic arm brace held together at the elbow by a moveable hinge welded so that the brace could bend only between 140°and 180°. Both devices enabled effortless movement of the arms, ensuring normal poker playing but preventing the wearer from touching any part of his face. If any of the restrained recipients needed his nose blown or scratched, assistance was given by a monitor.”
They then had them play cards together at these tables for 12 hours. (They also went through quite a bit of effort to prevent accidental contamination during e.g. mealtimes.)
So, across 3 rounds, there were 36 recipients − 18 restrained and 18 unrestrained. 10 of the restrained recipients and 12 of the unrestrained recipients were infected.
They also ran a different, fourth round, where they had 12 uninfected guys play cards using “freshly contaminated object” (“cards, poker chips, and pencils”) from infected donors playing other games concurrently, swapping out the objects every hour for maximum freshness. They forced those guys to perform “exaggerated hand-to-nose and facial rubbing, often with conjunctival and nasal mucosal contact” every 15 minutes, because “it seemed the recipients were actively avoiding any contact to their faces”. None of those guys were infected.
This seems like substantial evidence that under more “realistic” conditions[9], transmission via fomites is not overwhelmingly likely for RV-16. I’d be more hesitant to update very hard without the fourth round, but they had a bunch of guys spend 12 hours playing cards that had been very recently and actively used by a bunch of sick people, and none of them got sick.
This paragraph was somewhat alarming (bolding mine):
The complete absence of RV16 on the fomite recipients’ hands was surprising. Certainly the nose-to-hand-to-fomite-to-hand-to-nose exposures of the experiment D (fomite) recipients far exceeded that of any normal indirect contact circumstance. Eight men with colds were contributing continuously. The cards, pencils, and poker chips used by these recipients were literally gummy from the donors’ secretions. Subsequent to the experiments reported here, we embarked on additional experiments studying the four steps (see above) of the contact transmission chain [12]. We found that the virus nearly disappears during the journey from the donor’s to the recipient’s nose. The donor may have thousands of infectious particles on his hands, but few are deposited on fomites; the cards and chips he handles often have no virus at all, and positive fomites have only 10-30 TCID50[10] By the time the recipient’s hands and nose are reached, the levels of virus drop to zero or nearly so. Significant quantities of virus will only reach their final destination if the mucus is still wet; evidently this situation happened infrequently or never in our poker games, even though the exposures were much exaggerated.
How does one square this with Gwaltney & Hendley, 1982? We don’t know how long recipients there waiting after the coffee mug handles were contaminated, but there was a 20 minute window between the plastic tiles being contaminated and the recipients touching them. That’s longer than the enforced 15-minute interval for face-touching here. A couple possibilities:
“often with conjunctival and nasal mucosal contact” might have been doing a lot of work. What’s “often”? If substantial contact with mucuous membranes is load-bearing, that could explain a very large part of the effect.
Maybe the secretions on the contaminated coffee mug handles and plastic tiles took longer to dry than those on the playing cards & poker chips.
???
Also, I think this does not do much to distinguish between small particle and large particle transmission, given the table size.
Meschievitz et al., 1984 ran six trials where they housed multiple donors (usually between 5 and 10) with multiple recipients (similar numbers), for varying lengths of time, ranging from 5 hours to ~6.5 days. They report:
The experiments described in table 3 are arranged in order of donor-hours of exposure (DHE; one donor in the experiment room for 1 hr equals one DHE; five donors in the room for 5 hr equals 25 DHE, etc.) because rate of RV16 transmission correlated in a nearly linear fashion with DHE (r = .926, P < .01). The correlation was nearly perfect when DHE was plotted logarithmically (r = .997, P .001; figure 3).
Their experiment design, in isolation, doesn’t give us much to go on for updating on various methods of transmission. However, this does seem like it lets us reconcile Gwaltney (1978)[11] and Dick (1987)[12] - the longer you’re in close contact with someone sick, the more likely it is that they successfully cough onto your eyeball.
Other Factors
There are a couple of important factors that the above analysis doesn’t cover, that could substantially change takeaways. Briefly, those are:
Children. They shed a heck of a lot more of the virus, when sick[13]. All of these studies were on adults. If some methods of transmission have non-linear response curves, that might imply different things about how to prevent transmission originating with children than it would for adult-to-adult transmission.
There are many rhinoviruses (and many other non-RV “cold” viruses)! They could very well have different transmission characteristics. Who knows?
Review
Andrup et al., 2023 is a more comprehensive meta-analysis of the existing literature on the subject, which I held off on reading before I conducted my own research and wrote up the above analysis (minus the summary at the top). This is their conclusion:
We found low evidence, that transmission via hands and fomite followed by self-inoculation is the dominant transmission route in real-life indoor settings. We found moderate evidence, that airborne transmission either via large aerosols or small aerosols is the major transmission route of rhinovirus transmission in real-life indoor settings. This suggests that the major transmission route of RVs in many indoor settings is through the air (airborne transmission).
However, as far as I can tell, the only studies they analyzed which could plausibly support transmission via small particles (distinguished from large particles) were two studies on prisoners from the 60s. In the first one[14], researchers sprayed aerosolized inoculum directly into the subjects’ noses via a hand atomizer. In the second one[15], they “received aerosol inoculation by means of a molded rubber face mask attached to a cylindrical chamber containing a continuous flow of aerosol generated by a Collison atomizer”. All of the studies that tested conditions more similar to the real world found no transmission via small particle aerosols.
Conclusion
“Large” particle transmission: likely, especially over extended periods of time. (Remember, 10 of 18 experiment subjects were infected within a 12 hour period despite being physically restrained from touching their face with their hands.) “Small” particle transmission: not very likely (maybe even “very unlikely”). Fomite transmission: possible, but the strongest evidence comes from studies that are testing pretty contrived[16] setups, whereas the studies that check more natural conditions don’t see very high rates of transmission against the aerosol baseline. My guess is that in practice, fomites are probably not responsible for most adult-to-adult transmission. (I’m much less confident about children.)
Definitely avoid coughing or sneezing into people’s faces. Wash your hands before touching your face, if you’re taking care of a sick person… but don’t forget to use that paper towel to turn the water off, since faucet handles are hotbeds of other people’s germs. Face-to-face conversations seem much worse than ambiently hanging out in the same room.
Overall confidence: low. Reasonable people might not agree with my inferences about the likelihood of “natural” transmission via the three transmission methods described and tested by these studies. Might generalize poorly to children. Might depend on details of specific viruses, and I don’t think we’ve done enough research to have meaningful evidence about whether different RVs have very different transmission profiles from each other.
Thanks to Elizabeth van Nostrand and eukaryote for feedback on clarity. Remaining imprecisions are my own.
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Like being in the same room as someone for a while.
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That I could find!
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The authors note:
The aerosols produced by this method were assumed to contain particles of both large and small diameter. However, the method was characterized as “large particle” since this was the only contact situation in which passage of large droplets of respiratory secretion between donor and recipient could occur.
However, they don’t define “large” or “small” particle sizes anywhere.
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The study authors note that the “one infected recipient in the large particle aerosol group had had intimate contact with a hand-contact recipient on the evening of the first day of their exposure to the donor.” There are some other details here which suggest the study authors think the transmission was probably still the result of the tested transmission route (large particle) rather than via this unintended side-channel, but it does muddy the waters.
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I’m more interested in figuring out indirect transmission via shared surfaces (i.e. doorknobs, shared food serving utensils, etc), as well as “survival” time on various surfaces (including one’s own fingers).
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The study was simultaneously testing the effectiveness of spraying surfaces with a disinfectant. I omit discussion of those results for brevity.
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The researchers eluted the virus from the subjects’ fingers, and then used some plaque assays to test the eluates (by culturing).
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In this study, they used RT-PCR to test for presence of the virus.
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Though still exaggerated: “The average number of hand-to-face contacts recorded (186) over a 12-hr period was far in excess of that observed during normal adult behavior [7]: one “nose pick” every 3 hr and one “eye rub” every 2.7 hr.”
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50% tissue culture infectious dose, which works by progressively diluting a virus sample until a specific dilution infects 50% of separate “wells” of cell culture samples in a “plate” (a collection of wells).
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Only 1 out of 12 recipients sitting together at a table with infected donors were infected, despite high-risk activities like talking, singing, sneezing, and coughing.
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10 of 18 recipients, restrained in a way that prevented them from touching their faces, were infected from 12 hours of playing cards at the same table as infected donors. (Also 12 of 18 unrestrained recipients.)
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As infected children appear to have a higher viral load than adults, this may explain why children are considered to be the main transmission vector.
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The viral load in the mucus of more than 1000 rhinovirus-infected children below 1 year of age was 5.79 × 10e6 TCID50/mL, which is 10 to 100 times higher than our HC of 1 × 10e5 (Regamey et al., private communication)
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And fairly pessimal, for the recipients.
Obviously human trials of diseases are difficult to do in general, but studying transmission of colds is particularly difficult because “the common cold” isn’t one virus genus, or even one virus family. Wikipedia notes:
Certainly, many types of virus responsible are basically only transmitted via surfaces, but obviously COVID can be transmitted by aerosols. There are almost certainly some kinds of “common cold” that can be transmitted by aerosols, too. But it’s not feasible to do human studies of so many virus types—consider how hard it was for society just to realize that COVID was transmitted via aerosols!
Given the context above (posted by bhauth), the problem seems intrinsically hard. What would make this a civilizational failure? To my eye, that label would be warranted if either:
in alternative timelines with the same physics and biological complexity, other civilizations sometimes figured out transmission. If the success rate is under some threshold (maybe 1%), it suggests variation in civilization isn’t enough to handle the intrinsic complexity. (This option could be summarized as “grading on a multiverse curve”.)
deaths from the common cold (cc) met the criteria of “catastrophic”. The cc costs lives, happiness, and productivity, yes, but relative to other diseases, the “catastrophic” label seems off-target. (This option is analogous to comparing against other risks.)
Yep, that is a big question mark that I note in the conclusion:
(And also implicitly in a few places within the body of the post.)
I think it’d be reasonable to apply a large discount to any updates you’d otherwise make on the question of rhinovirus transmission from this post, at least absent a follow-up investigation re: whether they behave similarly or not.
It was only hard because inexplicably no one bothered checking for over a year into the pandemic, we just took the whole “fomites and large droplets” stuff from cold and flu for granted despite the evidence being as we see here pretty scant. There’s a serious coordination problem there IMO in how chaotic research ended up being rather than exploring systematically and rapidly all these very obvious things that we should have had some decent evidence on by April/May 2020.
If the mucus still being wet matters for transmission, failing to control (or report?) room humidity sounds like a big deal; that’s the difference between objects drying in minutes vs approximately never. Though also hard to square that with dry winter conditions being prime cold and flu season. Something like the virus needs moisture to live but also your mucus (and/or related tissues) needs moisture to work as a barrier at all?
The humidity thing is a good catch. I think there might’ve been one or two studies which investigated some related questions and reported some information about humidity, but I didn’t go very deep on them. Maybe a mistake!
Yeah, that’s an interesting consideration which came up in discussion with someone yesterday. Another possibility is that people congregate indoors more during wintertime, but I haven’t looked into that specific question. (It wouldn’t surprise me if someone had looked into it during COVID.)
I could also imagine it being the case that viruses are much less likely to be transferred from one patch of dry skin to another patch of dry skin via normal contact, than they are to be picked up by whatever mechanisms are used in various studies to check for the “presence” of viruses on surfaces. In several cases, this was approximately “dip fingers into some kind of liquid solution, then culture whatever was picked up in that solution”.
Unfortunately, the disinfectant results from Gwaltney & Hendley, 1982 point in the opposite direction:
The reduction in lab detection of viruses from the plastic tiles after being sprayed with a disinfectant (and then left to dry for 10 minutes) was much larger than the reduction in people getting sick after rubbing their fingers on the disinfected tiles (vs. non-disinfected tiles), and then rubbing their eyes/nose.
I expect this sort of thing to be quite sensitive to object-level details, and the sample sizes here aren’t huge.
Huh, more questions than answers there. Not a biologist but I’ve got to think there’s an easier way to study the surface transmission part than with live virus. If we’re assuming that: the virus is basically inert on surfaces and can’t move or divide or do much of note; transmission is just a function of how much intact virus makes it to the recipients tissues; then that should let us factor out studying how a ball of proteins about that size move through the environment from actually infecting people. And there’s got to be an easier way to test—add a marker to something that’s still a decent virus analog, like splice in a florescent protein or something that you can just see at a glance “how much”, but it’s still a protein that can denature at a similar rate. I’ve heard of demos like that using glitter or chemicals to show surface transmission, but that doesn’t capture degradation and has too many other differences.
The degree to which the virus is potentially degrading in the environment just sitting there is also a big confounder—how much did it degrade while waiting for the test vs before you took the sample? So something that let’s you test instantly seems worth a little extra fuss.
At the risk of being some 40 years late with my critique, that quotation has some problems.
First, if the relationship between two quantities A and B is linear in a semi-logarithmic plot, that generally indicates that the relationship between A and B is nonlinear, very boring edge cases aside! “I have one model which explains my data well and another which explains my data ‘nearly perfectly’” seems a bit of a strange message.
Also, arguing from models of infection, it is almost certainly wrong. The simplest toy model I can think of is “per DHE, every uninfected, susceptible person has a fixed probability of getting infected”, which would lead to an exponential decline of healthy individuals as DHE increase. But if that was the case, the curve should be bent linear if plotted with logY (when counting survivors), not logX. (I think the direction of curvature would be the same—highest infection risk per DHE at low DHEs, then a slow decrease.)
To explain why the distribution would look like observed would require a more complex model. For example: “Every uninfected person has a fixed personal exposure threshold when they become infected. It ranges from 45 DHE to 600 DHE and is exponentially distributed (favoring smaller thresholds) over the population in that range.”
If this was true, that would be highly surprising. Unlike with the killbots in Futurama, there is no good reason why your immune system should have a preset kill limit for RV16. If it is a case of “the immune system can fight of low doses but eventually gets overwhelmed”, then I am surprised that it would get equally overwhelmed by a low dose over a long period and a high dose over a short period.
I am also amazed that a study based on infecting people with cold viruses was run with so great a sample size that I can not spot the error bars with my bare eyes. Whom did they have on their IRB?Realistically, error bars are important. If you 100 percent are five out of five, that is very different from your 100% being 1000 of 1000.I agree that, considered from a mechanistic perspective, the obvious explanations for this data would be “surprising if true”. My guess for the actual model of infection is “did a sufficient quantity of the virus end up in contact with a non-protective surface like a mucuous membrane”, where “sufficient quantity” might vary by individual but for which “per DHE, every uninfected, susceptible person has a fixed probability of getting infected” is often a reasonable proxy (though it loses the details that might actually be relevant for more narrowly intervening on transmission). But I find it hard to be very confident, given the state of the available evidence.
Interesting post! At the Nucleic Acid Observatory we reviewed how easy it is to detect virus nucleic acid in air. Maybe of interest. https://www.sciencedirect.com/science/article/pii/S0021850225000266
The effect of humidity is particularly interesting (as it changes the survival time of aerosols—e.g., very dry air makes particles smaller, making them stay airborne for longer).
One potential argument in favor of expecting large-particle transmission is, “Colds make people cough and sneeze. Isn’t it likely that the most common infection that causes coughs and sneezes would also be one that spreads easily via coughs and sneezes?”
But I’m not sure how much evidence that really provides. I’m curious what others think.
The vibe I get, from the studies described, is reminiscent of the pre-guinea-pig portion of the story of Scott and Scurvy. That is, there are just enough complications at the edges to turn everything into a terrible muddle. In the case of scurvy, the complications were that which foods had vitamin C didn’t map cleanly to their ontology of food, and vitamin C was sensitive to details of how foods were stored that they didn’t pay attention to. In the case of virus transmissibility, there are a bunch of complications that we know matter sometimes, which the studies mostly fail to track, eg:
Sunlight can be a disinfectant, so, whether a surface or the air of a room can transmit a virus might depend on whether it has windows, which way the windows face and what time of day the testing was performed.
Cold viruses are widespread enough to have widespread immunity from prior exposure. Immunity might not generalize between exposure methods; ie, maybe it’s possible to be immune to low-quantity exposure but not high-quantity exposure, or immunity on nasal mucus but not deep lung, etc.
There are a huge number of viruses that are all referred to as “common cold”, with little in common biologically other than sharing an evolutionary niche.
Because immunity fades over time, there might be an auction-like dynamic where cutting off one mode of transmission still leaves you with recurring infections, just at a longer interval
I think that ultimately viruses are a low-GDP problem; after a few doublings we’ll stop breathing unfiltered air, and stop touching surfaces that lack automated cleaning, and we’ll come to think of these things as being in the same category as basic plumbing.
I am being lazy and not reading all the papers you referenced—do many of them discuss the viral load of the person who is infected?
I worked on PCR covid testing during the pandemic and the viral load of samples that went through our labs would often be multiple orders of magnitude different between samples. Some people seemed to just have way more virus in them than others, it did not obviously correlate with symptoms.
I was likewise very shocked at just how little was known about how virus actually spread on a practical level. How do people not know whether humidity affects how long virus remains active?, temperature?, dry vs wet surfaces?, rough vs smooth?, recently disinfected?, plastic/metal/material?, daylight (UV) vs artificial light, which of these factors is true regardless of particular virus?
Working with viruses is (I am told, I no expert) very hard—but I agree completely that this is an area that seems woefully underfunded vs related areas. I would be surprised if there were not cheap and effective 80⁄20 effects here that could be used to drastically cut infection rates in real world scenarios.
I am not that close to any of it any more and maybe it has, but I have not seen any of the post-covid enquiries raise this knowledge gap either.
I think a couple of them did; I don’t remember if any of them found strong effects. Might ask a language model to check later—agree that this seems like one of those big open questions that could imply huge differences in worthwhile interventions, though I think that if viral load turns out to be the only key factor in transmission likelihood, such that other interventions have basically no effect if effectuated w.r.t. spreaders with high viral loads, that’s pretty bad news, since testing for high viral load might be much harder/more expensive than e.g. putting on a mask if it turns out that “large particulates” are most of the problem in the case of a specific illness. (Though I guess we do still have the problem of knowing what illness a given person has, to know what intervention to apply...)
Curated. The OP said it right:
If I were listing out facts about humanity that would convince aliens we’re pretty primitive, this should be up there. Having better knowledge wouldn’t even require fancy conceptual breakthroughs, just creating some controlled conditions and measuring things. Or just measuring things comprehensively for a while.
So, curating this piece as a step in the right direction. This might not get solved before AI can figure it out all from first principles, but it feels better for not all of us to simply accept cold happens.
+1 to turning off faucets with paper towel (and the same for door handles in bathrooms).
I’m confused by the section headings.
“The large particle test” and “The small particle test” you write about under “Fomites” seems to be about Aerosols.
The experiments described under “Aerosols” seems to be either about mixed transmission or Fomites only. Passing around cards and poker chips, etc.
Am I missunderstanding something?
Seems like it’s fixed now
Hm, no, I didn’t change anything. The section headings are meant to indicate which transmission method those studies decided was substantially responsible for spreading colds.
So the section headings are not about the transmission type investigated, but which transmission type the studies pointed to as the leading one?
There is always the question of whether to study things bottom-up or top-down. These are bottom-up studies of what to do if you have a single infected patient. If you had an individual infected with a novel cold, that would be important, but we are generally interested in epidemics. In particular, why do colds go epidemic in the winter? We know there must be some environmental change. Maybe it’s a small change, since it only takes a small change in reproduction number to cause an epidemic. Then these controlled experiments might identify the main method of transmission. But maybe the change from summer to winter is a big change that swamps the effects we can measure in these bottom-up experiments.
What disturbs me more than the fact that the transmission question hasn’t been settled yet is that public health policy still seems to assume, even after Covid, that fomite and droplet transmission are the only ways for the common cold (and other respiratory viral infections like the flu) to spread, entirely ignoring the possibility of airborne aerosol transmission.
Even without definitive evidence of how a particular strain of common cold virus is transmitted, we know that respiratory viruses can only spread through three possible routes: fomites, droplets, and aerosols. So, the missing piece of public health advice, besides washing hands (for fomite protection), is at least to wear a respirator (for droplet and aerosol protection) or isolate during a bad common cold (or flu) season. Eye protection can also considered, though transmission via the eyes is probably much less common.
Personally, I lean more toward airborne aerosol transmission, because it seems that a bunch of stuff needs to line up just right for fomite and droplet transmission to produce fast and significant spread. For instance, coughing or sneezing into someone else’s face doesn’t seem likely to be a common occurrence to me.
But would knowing the correct route of transmission make any significant difference for the public? Would most people start washing their hands more than they do today? Would they start wearing respirators or isolate at home for months? I doubt it; they’d probably only take extreme measures if the threat was perceived to be extreme, something at least as deadly and as transmissible as Covid. Still, some people (the elderly or people with compromised immune systems, for instance) might want to take some of these more extreme measures. It may also help the broader public get used to the idea of wearing respirators during a bad pandemic in order to avoid disruptions, such as lockdowns, that occurred during the Covid pandemic.
I’m very confused. Reading this confirms to me that we know quite a lot about how colds spread? Coming from a physician perspective, and relative to our level of knowledge about most diseases, this sounds like pretty damn good knowledge...
It spreads through body fluids the more direct the more transmissible
I think there’s at least a few senses in which “we” don’t “know” how colds spread:
The “state of the art” in terms of “scientific knowledge” seems slightly underconfident about small-particle transmission maybe not being a meaningful factor in practice, given the available evidence.
As a society, I don’t think there’s well-established common knowledge of our best guess of the relative likelihood of transmission by various routes. i.e. what would happen if you asked multiple different doctors (GPs) how to best avoid catching a cold in various situations? I, personally, expect that you’d get overly-broad (and therefore expensive-to-follow) advice, with relatively poor inter-rater agreement, compared to if you asked them how to avoid e.g. some specific STDs.
Our “best guess” is extremely flimsy, and the sort of thing that I could imagine a single well-designed, medium-sized study overturning. (See the various caveats about how many different viruses cause “colds”, questions about humidity/viral load/etc in other comments, and so on.) This is not the kind of situation where I can tell someone “do [x] and you’ll reduce your risk by 80%” and feel at all confident about it! Or, like, I can in fact give them an extremely broad [x], but in that case I’m pretty sure that I’d be destroying a bunch of value as a result of empirical uncertainty which seems in-principle quite possible to resolve, with a sufficient application of resources.
Wild guess: air temperature and humidity should make a big difference in how quickly things dry. As hands are constantly sweating, I could imagine that there is a kind of threshold humidity/temperature beyond which hands have enough moisture to sustain viruses?
My personal theory, based on personal observation, is that it does not “spread,” and no one “catches” it. The reason it appears that it is spreading is because a group of people are often exposed to the same environment. So how do we know what I am saying is true? Well, take a person who’s ill and expose them to healthy people in a healthy environment, ( not the other way around) and often they do not fall ill. I believe experiments have been done in animals and humans along the lines of what I just mentioned. While viruses/bacteria are certainly involved, they come at a later stage. If viruses/bacteria are implicated as the causative factor, then one ends up in a perplexing situation where one has to resort to ever more complex explanations of immunity and transmission.
As a general rule, a cold (or most acute diseases) is caused by trauma. In the case of the cold, it’s normally bad food; other causes are getting drenched, bad/contaminated air, radiation, etc.
Don’t be absurd. As eminent physicists have argued, influenza viruses fall from space; clusters aren’t due to mutual infection, but at simply having all been at the epicenter of a major fall together.