Also keep in mind that running an immune system is expensive and even somewhat risky. And the right alert level for your immune system is a result of many trade-offs.
Your idea of acclimatization would suggest that human immune systems' might also run on different settings in different places.
The entrainment / waning immunity mechanism can't explain chickenpox seasonality, since people generally don't get chickenpox (primary VZV infection) twice. So something else must be going on.
New people are born who are vulnerable. Eventually there are enough of them that you get a burst of infections until their numbers are reduced. That burst happens in winter because reasons above.
The school year seems like the most likely suspect for chickenpox seasonality. The overwhelming majority of adults are already immune to chickenpox, so most of the vulnerable population is mostly school-age children. Schools provide a prime ground for chickenpox to spread, with large numbers of low-chickenpox-immunity demographics spending 30-ish hours a week cooped up in close contact with one another.
If chickenpox mainly spreads at school, then we'd expect a spike and fade at some point during the school year as it starts circulating at high levels and then burns itself out. Then it fades even lower starting in May/June when the schools close for the summer. Then in September, schools start up again with a fresh cohort of kindergartners joining the population. It would presumably take some time for residual cases to multiply into a spike, triggering the cycle once more.
I got chickenpox during elementary school years. My younger sister caught it in preschool, though. But that only gives a sample size of three.
I looked it up, and it seems like as of 2006 (when the vaccine was available but still ramping up in adoption), the peak age cohort for chickenpox infection was 5-9 years old.
That might be the driver for other seasonal diseases too. I know I never got sick nearly so often as I did after I had kids in school. I wonder if you can find somewhere that the school year isn't synched up with the flu season.
"In Figure 5, the LSF curves for all prefectures except Okinawa (Fig. 5h ) demonstrated a bimodal seasonal cycle with a first peak in winter (December–February) and a second peak in spring (April–June)."
So the start of the school year does not explain Okinawa. Also, according to this study, Canda has also the peak in Spring, not Winter. The study obove explains the two peaks with temperature.
Well, to be fair, the school year starts in April, then they have August off, then starts back up in September till July. So Japan has school year round, save for one month. Only the official year starts in April.
That does throw a wrench in the notion that it is all primary/secondary school driving things, however. College matches the western winter norm, but I doubt there are enough college students to drive things as effectively as school aged kids.
Yeah, I'd expect K-12 schools, especially elementary schools, to have a much bigger effect than colleges, for three reasons:
1. Younger children would be more immunologically naïve than college students.
2. Young children tend to be notoriously slapdash about the kinds of hygiene that reduce the risk of contagion, at least for diseases spread through fomites, droplets, and casual contact.
3. School-age children tend to live with their parents and (for younger children) have a ton of close casual contact with them, allowing a nice wide avenue for diseases to spread into and out of the adult community. Whereas college students tend to be much more sequestered in their respective campus communities, often living, dining, and doing most of their social activities either on campus or in nearby establishments that specifically cater to college students.
Anecdotal, but in the childcare services I work at, that's how it goes. New year starts in September, so heading right into the autumn/winter season. Colds go through everyone, including the staff, because if one kid gets it, everyone gets it. Ditto with other infectious diseases, so that's why we have a policy on "if the kid gets sick while attending, the parents are called to pick them up; if they get sick at home, they can't come in for 48 hours (until we know if it's communicable/they've stopped throwing up and pooping)".
Not sure how anyone would know at this point, but what's a seasonal COVID world look like? Are we talking death counts like 1) seasonal coronaviruses 2) RSVs 3) Influenza 4) Worse?
Assuming the two new pills work as reported, they drop the death rate by about an order of magnitude. So does vaccination or natural immunity from getting the disease. Combine those and the death rate is down by about two orders of magnitude, which I think gets it to or below the death rate from flu.
Do the new pills work specifically against Covid, or against all RNA viruses? Because if it's the latter, they could also reduce flu mortality by an order of magnitude.
Quoth Wikipedia: "Molnupiravir was originally developed to treat influenza at Emory University by the university's drug innovation company, Drug Innovation Ventures at Emory (DRIVE), but was reportedly abandoned for mutagenicity concerns."
Since the pills have to be taken early in the course of the disease (and generally before symptoms are bad enough to be scary) real world population effectiveness will depend on things like how likely people are to test, how easy it is to get from a test to a prescription in three days, compliance with the course (currently something like 40 pills in five days, though that often gets better as drugs are improved), etc.
My sense is that it will help quite a bit, but, especially in a world where there's a lot of disagreement about how serious Covid is to begin with, a lot of people won't bother with it until it's too late. (Or will find closing the test to pills in hand loop too slow, especially if they're not fast off the dime to get tested, or test results are slow to come back.)
I think that is where the efficacy will fall down - you have to take the new pills early. But how can you be sure that you have contracted Covid, rather than a cold? And testing is backed up because of the sheer numbers of people all wanting to get tested plus officialdom not accepting "I used a test kit I bought in the supermarket".
So you could have people panicking and running to the doctor for the new pill when it really is only a cold, and people waiting until the symptoms do get worse by which time the intervention is less effective.
It will be coordinated with the pharmacy. You won't need doctor's prescription as pharmacists in many countries are increasingly given power to assess the patient and provide prescription drugs. Ideally if you are symptomatic, you can get tested at the pharmacy and if positive, you can get your 5 day course of medicines there. Possibly even insurance paying for it, if you fulfil all criteria such as belonging to a risk group, of certain age, any comorbidities etc.
It includes the US. Pharmacists can already do vaccinations in the US and vaccines technically are classified as prescription only. The scheme to dispense Paxlovid is entirely planned in the US.
Well, one clue is the age gradient that it attacks. I'm no virologist, but COVID looks more like the cold than the flu in how it treats younger demographics, so in its fully endemic form, you'd expect it to be more like a seasonal coronavirus than the flu. But I have no idea of course.
I don't think it's unreasonable to hope thar thanks to spillover of state of the art vaccines from Covid to flu and RSV, as well as cross-immunity between Covid and endemic coronaviruses, that the net risk of dying from any of those pathogens could drop significantly within the next decade.
According to ONS's regular survey in the UK, >97% now have antibodies in the age group 50+. This means, they're more or less in the endemic stage now. Their daily COVID mortality numbers since late August ranged from 1.5 per million to 2.5 per million. Annualized, this yields the range [540dpm, 900dpm]. Assuming similar numbers for the US, this would mean something like 150k to 300k extra deaths per year, every year. To put this in context, CDC estimates yearly flu mortality burden to be 10k-50k from 2010 to 2020. So looks in its endemic state, SARS-2 won't be "just another cold", nor "just another flu", but rather, a nasty nasty (~5x worse) flu noticeably burdening the well being of the public.
Peru is about to hit 0.7% population excess mortality, so they must be at comparably high seroprevalence as the UK—meaning they too are probably at the endemic stage. Their flu season is from May to September, so they're not in flu season. They're currently recording ~1 COVID deaths per million daily. So 365dpm per year. Given their young demographic structure, this comports with our back-of-the-napkin calculation for the UK.
New vulnerable people are continually created though.
No idea about Syphilis but HIV did not become milder over time. We developed treatments for it. Of course, the same will be true for COVID, but who knows how effective that'll be overall.
It's true that the CDC estimate influenza burden at 10-50k. But the excess death toll of "flu season" is much higher than that, and on the order of 60-120k extra deaths every winter, depending on whether you use the summer or fall months for how many deaths there "should' be. The difference in the numbers is the causal of death. Many of the winter deaths are due to other non-influenza seasonal flu viruses or bacteria.
Also I agree with Matthias that a declining CFR is more likely than an unchanging or increasing CFR. That probably put the burden of covid much more inline with another "flu season", if not with influenza specifically.
For now, it's worth adding, that flu itself still hasn't returned to the US. And even weirder, from what I can see of preliminary CDC data the regular "flu season deaths"(the distinction being seasonal deaths that may or may not be influenza, specifically) have not returned either. In other words, if you take total deaths and subtract covid deaths, the usual seasonality in deaths has virtually disappeared since Jan 2021.
I don't know how long this unusual situation can continue, but for now it seems like covid is replacing seasonal flu deaths, and not adding to them.
> Many of the winter deaths are due to other non-influenza seasonal flu viruses or bacteria.
Yeah, Influenza Like Illnesses ("ILI"), and other endemic diseases.
> Also I agree with Matthias that a declining CFR is more likely than an unchanging or increasing CFR. That probably put the burden of covid much more inline with another "flu season", if not with influenza specifically.
I don't know about that. That reasoning strikes me as wishful thinking. After all, ILIs keep killing similar amounts of people every year: the dry tinder doesn't get exhausted.
> flu itself still hasn't returned
Yeah, that's very interesting. It would be very fortuitous if a class of pathogens went extinct as a happy side effect of NPIs. But I'm not counting on it, most of them will probably return in a couple of years max. But it will be fascinating to examine in what ways the cohort born in 2020-2021 are healthier than the general population. We'll possibly confirm pathogenic origins of some cryptically caused diseases, like type-I diabetes.
FWIW - Peru has had an unusually rough time with covid. (why: climate? living conditions? genetics? altitude? medical care?)
Their recorded mortality stats are way off the charts and 2x-4x all of their neighbors, which were also hard hit. Some of that may be they are much better at actually recording deaths. But it's worth cautioning that to some extent their worst-in-the-entire-world experience may not be extrapolate to the experience of other countries.
Peru switched to counting all excess deaths instead of just PCR confirmed ones, so they look horrendous compared to other countries where deaths are undercounted by 2-5x. Here are some known excess population fatality rates (calculated from official all cause mortality stats) as they stand currently:
Bulgaria 0.78%
Russia 0.67%
Peru 0.67%
N. Macedonia 0.6%
Serbia 0.59%
Lithuania 0.54%
Mexico 0.47%
Romania 0.46%
Keep in mind that Peru—having entered the endemic stage—is more less done with the pandemic, but many Eastern European countries are in the middle of their current waves.
Given that Mexico and Peru have similar age structures, 70% of Mexicans having been infected, and 100% of Peruvians having been infected is consistent with their 0.47% and 0.67% PFRs respectively. Similarly, South Africa's 0.39% PFR, and their pop pyramid means that they too must be close to 100% attack rate. So doesn't look to me like Peru is this egregious outlier: their outcome is entirely predicted from Levin et al.'s IFR(age) function under the assumption that almost 100% got infected.
If the confounding factors like temperature and UV are really just a small influence, I'd expect at least some diseases to start their cycle in the summer, just by chance. Yet basically all infectious deseases are peaking in winter.
Also, if the non-seasonality in the tropics is caused by import, we should see a similar cycle in other countries, since more people are travelling between the hemispheres than from either hemisphere to the equator (to be fair, that's just an educated guess on my part).
Lastly, the immunity cycle should not allow double peaks. While it might be possible that the immunity "expires" with an offset of half a year for half the population, it would be far harder to actually peak for the virus since half of it's targets are already immune. Due to these network effects, I'd expect a wider curve instead of a peak.
That theory looks good, but I think we're still missing some pieces.
Double peaks for flu come from the fact that there are many strains and while immunity to a given one might last for years you can be exposed to a completely different strain 6 months later if you're unlucky; I'm basing this off knowing that flu vaccines in the Southern hemisphere are based on which strains caused the most recent Northern winter flu spike, and occasionally miss entirely and do nothing at all against the dominant strain in the Southern winter spike, and extrapolating that years where that happens would seem very likely to cause a double-spike in the tropics.
>Also, if the non-seasonality in the tropics is caused by import, we should see a similar cycle in other countries, since more people are travelling between the hemispheres than from either hemisphere to the equator (to be fair, that's just an educated guess on my part)
Scott talked about the part of the article which discussed Australia (more specifically the Top End, ie Darwin and surrounds). Darwin is heavily touristy, so a pretty large fraction of the people there at any given time are coming from elsewhere in Australia, much larger than the fraction of people in any major temperate city who are coming from the opposite hemisphere.
There's some other details in that article that Scott glossed over though, it mentions different flu patterns in different tropical cities. Darwin usually has one peak but sometimes has two. Singapore has two peaks. Colombia has year-round flu transmission, and Fortaleza in Brazil usually has one peak.
This seems to line up with an import theory. Singapore has many visitors from both hemisphres. Darwin mostly gets visitors from the Southern hemisphere and fewer from the Northern. Fortaleza mostly gets visitors from the southern parts of Brazil, and Colombia doesn't get many visitors at all (for its size, relative to the other places mentioned).
“ Except in the equatorial regions, respiratory syncytial virus (RSV) is a winter disease, Martinez wrote, but chickenpox favors the spring. Rotavirus peaks in December or January in the U.S. Southwest, but in April and May in the Northeast. Genital herpes surges all over the country in the spring and summer, whereas tetanus favors midsummer; gonorrhea takes off in the summer and fall, and pertussis has a higher incidence from June through October. Syphilis does well in winter in China, but typhoid fever spikes there in July. Hepatitis C peaks in winter in India but in spring or summer in Egypt, China, and Mexico. Dry seasons are linked to Guinea worm disease and Lassa fever in Nigeria and hepatitis A in Brazil.”
Genital herpes peaks in spring/summer because its an std and more people are going out and thus having hookups in spring summer. Typhoid fever is salmonella based which as to do with with harvest cyles as well as meat spoling.
The point is not all diseases have the exact same factors which lead to the same cycles, there are variations based on individual characteristics and vectors of transmission. I dont have an exact model for this, but I don't this invalidates the basic hypothesis necessarily.
I think what you're missing here is that complex system dynamics with strong positive feedback mechanisms -- and a viral disease has one heck of a positive FB mechanism -- *often* exhibit large oscillations. You have only to think about stop-and-go traffic on the freeway. Where do those stops and goes come from? They will often seem to have no rational relationship to events on or the structure of the road (although we will all instinctively attempt to assign one, e.g. it was that nogoodnik in the #1 lane with an extra 20 feet of space in front of him). But these things, like water hammer in pipes, or predator-prey oscillations, Ice Ages probably, derive from dynamic instabilities in the system's evolution, and *don't* require any large effect to start or pace them. Even very small perturbations are enough to trigger large oscillations, and even very small nudges are enough to pace them.
Our intuitions about the dynamics of complex systems are often mistaken. So we expect there to be a big reason for why a thunderstorm happens now instead of 4 hours later, or why stop-and-go traffic develops here instead of there -- and why big oscillations in disease diagnoses happen in this month instead of that. But there can easily not be. It can easily be an instability of the underlying dynamics, with triggering (or pacing) factors that seem wholly insufficient in magnitude.
I mostly agree, but when I see a noisy dynamical system that exhibits pretty regular oscillatory behavior, this suggests to me that it is being driven by something with a similar frequency to its characteristic frequency. And I guess I'm a little surprised that so many diseases have characteristic times for increasing susceptible population that you see this level of seasonality? Especially if the system is (seemingly) not being driven very strongly?
Well, the problem is that seasonality affects everything on Earth, pretty much. The natural world (temperature, humidity, sunlight), the biological world (growing cycle, reproductive cycles of animals and insects), and us (we clearly exhibit seasonal variations in health, fitness, mood). So it's not at all surprising that *if* there are going to oscillations arising from underlying chaotic dynamics, they are willy nilly going to end up with some kind of approximately seasonal time constant. How could they not? There isn't any other important time in the system.
Not driven very strongly is exactly what I'm getting at. Unstable dynamical systems don't *need* a strong driving force, they can amplify a teeny tiny driving force so you get results that seem wildly out of proportion. Another example that comes to mind is electronic oscillators, which fall almost immediately into their extreme oscillation modes following undetectably small fluctuations.
That's why I'm saying when Scott says "hmm this driving force doesn't seem sufficientg" he's falling prey to the assumption that the underlying dynamics are stable, which is where our intuition naturally takes us. But they may not be -- indeed, I'd be quite surprised if they were, given the existence of the strong positive feedback loop in infection (the more people are infected, the faster new people get infected). That seems like an almost classical example of a highly unstable dynamical system, and the surprise would be if it *didn't* exhibit wild oscillations.
Yeah, I get that dynamical systems will spontaneously start oscillating in response to tiny perturbations (laser oscillators are another example of this). But getting them to stay in phase with an external driver over many cycles typically means that either the driver is strong or it is acting at a frequency close to the characteristic frequency of the system.
I do not think that 1 year is the only relevant timescale for an epidemiological system. Doubling time for many diseases is ~1 week, human behavior and biology have cycles on the scales of 1 day, 1 week, and 1 month, and some vaccines apparently only need to be boosted once every 10 years.
To be clear, I am not saying that this is mysterious or the driver must be strong. It's plausible to me that the dynamics of human diseases are such that all you need to see strong seasonality is for a population to regain susceptibility on any scale between a few weeks and a year, plus a weak driving influence with a period of a year. I just don't think "dynamical systems do this all the time" gets you more than "your prior on seasonality should not be very low".
Yes of course the natural frequency belongs to the infected population. But surely it can't be a surprise that the human population has natural frequencies that correspond to the seasons, right? Many such reasons have already been identified (crowding, sunlight) and I'm sure you can think of many more (nutrition, fitness, sleep, mood and self-care, school schedules). It would in general be surprising if oscillations in any aspect of human health did *not* have frequency components near the seasonal swing. (We know both births and deaths do, for example).
Sure, any driver has to have a frequency component near the natural frequency, but since most fluctuation spectrums are broad, this requirement seems almost trivial to satisfy. I would have a hard time thinking of any source of low-level fluctuating impulses that had a narrow-band spectrum. Can you think of any?
Your final sentence is in the direction I'm arguing, I would just make it far stronger: the nature of complex dynamical system is such that your prior on there being a clearly identifiable driver with (1) intuitively satisfying magnitude, and (2) matching narrow-band spectrum should be approximately zero.
But then I'm an empiricist, not a rationalist, and my prior on most plausible hypotheses on complex systems is zero to several decimal places. I've been surprised by such systems far too many times in practice.
> They will often seem to have no rational relationship to events on or the structure of the road (although we will all instinctively attempt to assign one, e.g. it was that nogoodnik in the #1 lane with an extra 20 feet of space in front of him).
Sure, but they also often totally have a rational relationship to the structure of the road -- a curve that's too tight for traffic to flow at its normal rate, a merge point, etc. Just like there's a traffic jam at the bend in the freeway every weekday at 5:00, we have flu spikes every winter.
Yes, those would be a different case. I'm talking about the apparently inexplicable stop-n-go business that happens in LA traffic pretty much all rush hour, along hundreds of miles of freeway, with no obvious relationship to the features of the road. But that's just one example, there's a vast cornucopia of unstable dynamic systems that develop wild oscillations from trivially small fluctuations.
I had the same thought. What if for example there is some remnant of winter hibernation in humans that we barely perceive, but has an effect on virus resistance. That would explain why the outbreaks happen in whatever people consider "winter", regardless of the specific weather.
The many articles I've seen on this topic in the past year and a half have had many theories, but none of them include a clearly correct explanation. The point is just that an explanation of one that predicts that all should have the same season doesn't seem likely to be correct, but an explanation that allows some variance between diseases might be more plausible.
I'm not a biologist, but the human body could well have adapted to learn something like "no need to keep immunity for more than six months" if it was costly to keep it for longer.
I doubt this applies to T-cells, where keeping information is very cheap, but might apply to antibodies, which are expensive to maintain.
I mean, moon phase corresponds to weak or strong tides in an incredibly strong way - I'd be shocked if "the tides are more aggressive" didn't increase drowning in those parts of the month?
Sickness waxes and wanes with the inconstant moon. There are (roughly) thirteen lunar months in the year. Thirteen is an unlucky number. This is why! 😁
“ I have never heard anyone claim that any winter diseases happen in summer in Arizona or Saudi Arabia or terrible places like that.”
We did indeed see delta surge in southern states at precisely the time when everybody was indoors with AC. Could’ve been coincidence, but we have heard of it.
The most obvious naive explanation to me seems that humans have some seasonal patterns in their biological activity - which would make sense for an animal evolved in non-equatorial regions - and those patterns affect immune system activity. Is there a straightforward reason why this explanation is so wrong it's not even worth considering?
Also, what about human adaptability? E.g., what if in whatever climate you live, your body is going to do just good enough job to maintain the right temperature (36.6 C or whatever) in your sinuses most of the year, but when the temperature is at the local minimum your sinuses temperature is going to drop somewhat, providing a comfortable environment for the virus. Local lows are below human body temperature pretty much everywhere, so this model would work everywhere, and the "slightly below the normal human body temperature" is independent of external temperature so we'll see about the same effects in every place with seasons. Is there anything obviously wrong with this model?
Why would your body have a program to make the immune system work less well at a certain time?
The body certainly adjusts its temperature on a moment-by-moment basis, but I don't know if there's evidence that it does some kind of weird long-term adjustment where it lets body temperature be colder whenever outside temperature is colder than its mean value.
>Why would your body have a program to make the immune system work less well at a certain time?
To save the energy during the [presumed] times of hunger in winter? One could counter by saying that it's stupid and body should regulate such things based on the actual availability of nutrients, but it's equally stupid that we get sleepy based on ten random external and metabolic cues and not just whenever we lie down and relax, yet here we are.
>The body certainly adjusts its temperature on a moment-by-moment basis
Right, and as far as I understand that includes adjusting the temperature down a notch when it's kinda cold. And even though for you living in the bay area "kinda cold" is +5C (outside) but for someone in Central Russia "kinda cold" is -25C, but in both cases the body adjusts just a bit and arrives to roughly the same lowered temperature. What I'm trying to articulate is basically "people tend to feel cold in the winter more often" (though I don't have any studies to quote on this one unfortunately).
When I said "hunger" I should've said "scarcity", winter means not only potentially lower supply of nutrients but also necessarily higher demand on them to maintain the body temperature.
My 10 seconds of thought answer: Would it make sense for your body to just plan on getting diseases every so often, to develop immunity, and synchronize it with times when you're mostly just sitting around anyway?
In our ancestral environment did we spend winter "just sitting around"?
Actually in our ancestral environment, did we have winter? Kenya is in the tropics. I don't know what its seasons are like.
What do we know about seasonality of viruses in other animals? I'm wondering about bats, famously disease-ridden mammals that, much like humans, spend their spare time hanging around in huge groups and sharing pathogens, and also conveniently live all over the world but rarely travel between hemispheres. Do their viruses have seasonality? If so it might help us eliminate some of the theories like "it's because people spend winter indoors".
_Unless_ some of the diseases can kill you, why bother to fight any of them? _If_ some of the diseases can kill you, how does your body know that those are the ones to fight(vs. just practice on)?
If it doesn’t kill you, but makes you less effective at getting the things that keep you alive, you want to fight it. Maybe that’s a way for it to “kill you”, but it’s not usually what we mean.
I don't follow. The poster I was replying to(Meefburger) was suggesting that possibly the human body _occasionally_ allows (some?) viruses to invade, so as to provide "exercise." My point was that there does not appear to be a method to evaluate viruses for lethality at-the-front-door. Thus this system would be very problematic and unlikely to have evolved.
Basically, biology is such a mess, that organisms actively rely on their imperfections, because evolution doesn't have a way to tell which aspects of us are features and which are bugs.
My current understanding is that "exposure" can not cause you to get a cold, but it can very well turn a flu into pneumonia. Walking around in the cold with an active virus is usually an unwise thing to do, especially if you have other risk factors. It may be that cold is triggering a "short term" orientation in the body - we're making sure things keep working now, and we'll restart the immune system tonight when we're warm and cozy.
I can also easily imagine other reasons for the same interference. Maybe lower overall blood flow may mean lower overall communication between circulatory and lymphatic systems. Or cold interferes in a mechanical way with immune cells properly reaching the respiratory system.
But yeah, this doesn't affect the main point: disease is a non-linear system that needs only small nudges to fall into a seasonal pattern.
This paper claims viruses adapt themselves to local temperature changes to maximize their chances of staying in the upper respiratory tract to maximize spreading.
The explanation I've always heard is that cold and wet both reduce our immune response because the body has to spend more energy dealing with the cold and wet. Many of us have heard our mother's say "don't play in the rain or you'll catch a cold."
On the other hand, my respiratory therapist wife has said that people are more vulnerable to respiratory infections in the winter because it's so dry that the protective mucous membranes in the airway dry out.
That only helps the relative humidity, not the absolute humidity (which will certainly help your skin and hair not dry out as much.)
It won't help your respiratory system much though; your lungs are very efficient at heating air to body temperature, so the relative humidity in the lungs is only a function of absolute humidity.
> Why would your body have a program to make the immune system work less well at a certain time?
I'm not a biology/medical person, but in women I understand that your immune system is suppressed during part of the menstrual cycle to promote pregnancy. Is there any reason why it would be better getting pregnant in the winter? Speculating wildly, but something to do with food availability?
I agree that although it might be a complex system, biological factors probably play greater role than suggested in the post. For example there is research that suggests that being cold dampens the immune system to some degree (https://pubmed.ncbi.nlm.nih.gov/10066131/), but there are other effects, for example that heating dries out the mucous membrane and probably there could be other factors as well. I think the idea in the original post that the virus only need to outrun itself locally compared to the summer was on to something. When we are combining all these factors it becomes very likely hat the virus will thrive in the winter compared to the summer. Why would it do the hard work in summer if it can wait for the far more ideal conditions in the winter?
Could the difference be us rather than the pathogen? Maybe people are more vulnerable in the winter for some reason. If you look at mortality by month for the U.S., it's high in the winter, low in the summer.
I responded elsewhere with a similar thought. Folksy wisdom has said for years not to play in the rain, for fear of catching a cold. Obviously you're not going to catch a pathogen playing outside by yourself, but it's probably still true as related to weakening your response to pathogens you have already been exposed to.
Viruses are pretty fragile. Somewhat simplified: you pretty much have to catch a fresh virus directly from a fellow human. Bacteria and worms etc can survive outside their preferred hosts for much longer.
I know I tend to get a runny nose in cold environments -- surely I can't be an exception in this ? Runny noses would contribute to the spread of seasonal viruses, IMO.
I'm quite sure this is a preventative measure to stop viruses from taking hold. Viruses already don't do well in warm air, and your nasal passages are the first thing to vasoconstrict in cold weather, meaning there's less warm blood going through and your airways are more vulnerable to infection. The runny nose tries to compensate for this by flushing them out instead.
I've personally noticed that, pre-pandemic, when I wear a scarf over my nose and mouth in cold weather, I'm drastically less likely to catch a cold. It's unlikely that a woollen knit scarf is stopping any viruses from getting through so I believe that letting the warmth of my breath circulate, instead of just escaping, is why it's harder to get sick.
> The runny nose tries to compensate for this by flushing them out instead.
It was counter-intuitive to me so it took me a long time to notice, but, yeah, when I am dehydrated my nose runs more. (My intuition would say that my body should be trying to save moisture when I'm dry.)
I don't have much knowledge on the subject but I'll toss out an idea that animals could have something to do with it, since there's a lot of animals that change their behaviors drastically based on seasons (mating, migration, etc.) Maybe some animals or insects develop some new disease variants over time, and seasonal behavior causes them to transmit it to humans. Though it would be disproved if a lot of these diseases don't originate from animal sources.
Animal reservoirs are important for some viruses, but when I looked up chickenpox, there are no corresponding animal/insect-to-human transmission. So that knocked that theory on the head for me, as chickenpox is apparently seasonal with most cases in winter/spring.
I dunno, maybe it has to do with when the stars are right!
1. No reason to choose this specific Australian study of the dozens of RCTs, just because it happens to be the most recent one. It's not like this is a constantly changing field.
It's a meta-analysis covering 25 RCTs, and it finds a significant protective effect, including a very strong one for deficient individuals.
2. It's not surprising the Australian study wasn't successful, since: a) It used bolus doses, which the meta-analysis also found to be ineffective (interestingly, both studies got almost the exact same effect and CI!); and b) It was done in a sunny country. You can see that the vit D levels of the controls (77.5 nmol/L) was higher than any country in Europe (mostly 40-60): https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4288313/#b5025
3. Nevertheless, the Australian study still managed to reach significance on duration and severity.
4. Most importantly, it's wrong to extrapolate from the effect of vit D on the individual to the whole population. Even if we accept the wrong conclusion that an individual has only a slightly shorter duration and viral load, the multiplicative effect of that as the virus goes through the population (20-30 generations?) could be huge. For example, 0.95^25 is 4x.
My personal impression is that vitamin D and close unventilated spaces are the main factors (note that in summer there is usually better ventilation).
May I be a bit lazy and ask you instead of digging through the sources? My current understanding is that vit D level is important, but for some (weird) reason it's much better if you got to that level by sun exposure than by (commonly available) supplements. Is that true?
Trouble with Vitamin D supplement is you are supposed to take it with a fatty meal. I never know when the next fatty meal arrives and when it is there I'm all over it without thought of any pills.
E.g., chickenpox is spring seasonal. (And as Metacelsus mentioned, an immunity-based mechanism can't apply to it.) And other diseases have other seasonalities...
To make things slightly more complicated, not all seasonal viruses peak in winter. When the US suffered from annual polio epidemics in the first half of the 20th century, they would come in summer. I'm not sure why this is (or if anyone knows), although I think it was spread by water and one factor might have been swimming in shared pools.
This would fit with the theory given here if polio just happened to have some different relationship to heat, humidity, etc.
> I think maybe they’re saying something like that getting a virus like this usually gives you about a year’s worth of immunity before your immune system “forgets” it
Does anyone know why the human immune system will forget certain viruses in a year, but retain a strong immunity to certain other viruses for a whole lifetime?
Likely the immune reaction is somewhat similar but the viral growth rate inside the host could be orders of magnitude different. (Difference is in the virus not the hosts reaction....)
There are different levels of your immune system. Your T-cells can remember forever at little cost, but those are kind of the last line of defense. (I'm not an immunologist or even a biologist.) Your active immune system is the first line and it seems like it needs some "exercise" every now and then to stay in proper working order.
Not only different levels, but entirely different aspects.
We have different 'parts' of the immune system for fighting worms (and other such parasites), viruses and bacteria. I don't know if there's an extra mechanism for fighting (pre-) cancer, but it wouldn't surprise me.
"If you came up with some multidimensional dryness-coolness-indoorness metric, then maybe places could be high on one or two in the summer, but the combined metric would always be highest in the winter everywhere.
This is possible. I just find it hard to believe that the place where this metric is highest in summer doesn’t even overlap with the place where the metric is lowest in winter."
I think seasonality can probably be explained by a combination of this multi-dimensional metric PLUS network effects and waxing and waning rhythms of immunity.
Network effects = Texas gets more winter infection because of spread from colder states in the North
Waxing and waning immunity = Texas gets more winter infection because immunity is high post winter / into summer months, but by the time the next winter rolls around immunity has waned. So there will be natural waves / a rhythm to infection.
I think this waxing-waning rhythm is why we're currently seeing an uptick in all non-COVID viruses. 18 months of lockdowns globally, suppressed non-COVID viruses (including gastro) to a much lower effective R and now that restrictions have eased, the effective R is higher than in a normal season. My paediatrician friend in the UK reports a severe several months of non-COVID viral infections post relaxation of lockdowns, particularly in children aged 18 months to 3 years, who have limited prior exposure (eg. a lot of deterioration of bronchiolitis). I've also seen a lot of severe bronchiolitis in my clinical work in Australia post-lockdown.
I also suspect more winter infection occurs due to resource-depleted individual immune systems - eg. kids from childcare (and their close contacts) get many viruses in a row in winter in part because immune responses are depleted by prior infections.
My guess is "sunlight deficiency" broadly. Modern humans are naturally sunlight deficient because we spend way more time inside than our ancestors did, and the deficiency is much worse when days are short — so we should expect things to go particularly wrong in winter.
In this model, disease susceptibility could be mediated by any number of factors: vitamin D, nitric oxide, circadian rhythms...
I'm also confused by Scott's argument against vitamin D. I mean his fourth point on Why Vitamin D Doesn't Work is literally, "Black people have less vitamin D and oh wait, they actually do catch the flu more often."
Also note re: Vitamin D, African-Americans are horribly vitamin D deficient and do/did catch COVID far more often and more seriously than whites. This part of the case feels really quite weak as a consequence.
Also note the case of Sweden. Much better outcomes than the rest of Europe, a fact that pro-lockdowners are constantly trying to obfuscate by refusing to look at data from outside of Scandinavian countries. They claim the Nords are some sort of alien race whose culture magically wards off COVID and cannot possibly be compared to anywhere else in Europe - presumably many of these people have never actually been to Sweden - so actually Sweden did badly. But their culture isn't actually the same, partly because Sweden has such disproportionately huge numbers of migrants from Africa. Who, guess what, are all horribly Vit D deficient compared to the Swedish population.
Overall I really didn't follow the argument as to why Vit D is so clearly the wrong answer. When you add back in the evidence that wasn't included, it does seem at least highly plausible.
Pretty sure his argument is mostly based on priors; vitamin D *notoriously* has false positives for helping with everything, so some positive results are expected regardless of whether its helpful (and should be discounted as evidence accordingly.)
When I think about this, I usually attribute it to holidays. I know its very US-centric to think of it this way, but you have Halloween followed by Thanksgiving followed by Christmas followed by New Years it comes out to a lot of times where people will travel to visit family and possibly spread diseases to new areas.
But I have all the medical skills of a wireless Xbox 360 controller, so I'm going to pretend its Vitamin D just like everything else.
Additional factors that might make people have weaker immunity in winter:
* fewer fresh fruits and vegetables available to eat
* less exercise
* exposure to cold temperatures weakening immune response by systemically raising cortisol levels and causing vasoconstriction that makes it harder for white blood cells to move around.
Seasonality of Respiratory Viral Infections, Miyu Moriyama et al, Annual Review of Virology 2020
"The seasonal cycle of respiratory viral diseases has been widely recognized for thousands of years, as annual epidemics of the common cold and influenza disease hit the human population like clockwork in the winter season in temperate regions. Moreover, epidemics caused by viruses such as severe acute respiratory syndrome coronavirus (SARS-CoV) and the newly emerging SARS-CoV-2 occur during the winter months. The mechanisms underlying the seasonal nature of respiratory viral infections have been examined and debated for many years. The two major contributing factors are the changes in environmental parameters and human behavior. Studies have revealed the effect of temperature and humidity on respiratory virus stability and transmission rates. More recent research highlights the importance of the environmental factors, especially temperature and humidity, in modulating host intrinsic, innate, and adaptive immune responses to viral infections in the respiratory tract. Here we review evidence of how outdoor and indoor climates are linked to the seasonality of viral respiratory infections. We further discuss determinants of host response in the seasonality of respiratory viruses by highlighting recent studies in the field."
> Some people get the disease, it spreads exponentially until lots of people are immune, and then it stops until something changes.
Isn't it a problem for this theory that most people _don't_ get flu in any given flu season? In a typical flu season maybe 1% of the population gets flu, this isn't enough to meaningfully change the overall population immunity.
Possible counterpoint: most people do have some degree of flu immunity at any given time due to exposure to other strains. Each year you've only got a few percent of the population actually susceptible to getting flu; a wave of flu comes through and infects a third of those; now you're back to 98% immunity instead of 97% and that's enough to put the R below zero for another nine months or so.
Alternately, many people get the flu, but an asymptomatic case. Felt a little run down one Sunday? It wasn't a late night at the bar, but a minor case of flu. Regretting eating at Taco Bell? Flu, not food poisoning. Thought your kid picked up a bit of a cold at school? Bit of the flu. Etc.
Flu cases very rarely result in people actually going to the doctor and getting tested, even when they get a case bad enough to stay home from work or school. The CDC has (up till last year at least) given a range of flu deaths of +100% the official estimate, because frankly no one knows or bothered to check much to confirm what people died of if it seemed natural. If you don't wind up in front of a doctor who does the test, no one ever knows you had the disease.
Its 10% infected per year, so substantial chunk of vulnerable population. Hard to know what true R0 of flu is given people have some form of immunity, but Spanish flu averaged 1.8, so need 45% infected for herd immunity (estimated to actually have infected 35%). Given some people likely will still be immune after a year, 10% is a huge share of vulnerable population and likely create temporary herd immunity.
I think we need to say that at least 10% of the population are infected by flu; we don't know the upper limit because we don't test enough to know since many people who get infected don't know and don't get tested. We just know how many get tested and turn out positive out of the entire population.
You only need to test a representative sample. The size of that sample is independent of the size of the population.
The last sentence might seem counterintuitive, until you remember that you only need to sample your suspicious dice a finite number times, no matter how large or even infinite the potential number of times you could roll them is.
I don't know, if anyone is doing random sampling for flu prevalence testing.
I understand the statistics. What I am saying is that we don't randomly test people for the flu, we test people who go to the doctors and get tested, either because they have flu like symptoms or the office just tests everyone. So we do not have a representative sample, we have a very biased sample, only those who decide to go to the doctor and see if they have the flu. Our sample is dependent on both people getting the flu AND deciding to go get tested, where what we care about is how many people get the flu, regardless of whether they decide to get tested.
To put it another way, we have the survey problem. Say you want to find out how many people have jobs in a town. You go to the mall some Tuesday morning and interview the people there, asking "Are you employed?" You are going to get a biased sample, the answer probably biased downwards, because you are not getting a representative sample of the town people, but rather a sample of people who happen to be in the mall on a Tuesday morning. The people in the mall on a Tuesday morning are less likely to have jobs than the general population, because people who have jobs are more likely to be at them than at the mall.
Most of our medical testing for diseases that have wide ranges of symptom severity, and thus a wide range of people getting them checked at a doctor, suffer the same issues as surveys in general. We can't get a representative sample of the whole population without a great deal of expense and time. At least we don't have as much of a problem with social desirability bias as with regular surveys.
Perhaps covid seasonality is somewhat dependent on the seasonality of other winter ailments like cold and flu. covid is just the one you get tested for most when you have cold- and flu-like symptoms. So maybe seasonality of other diseases causes more covid testing, which causes more covid positives "cases", the relative number of which is somewhat independent of the absolute level of covid infection in the population.
You know, I hadn't thought of that, but yea that would totally screw with using case counts as as estimate for actual cases. Damn, very clever! Where's the like button ...
I suppose you could mitigate that a bit by comparing deaths, but even then, all the seasonal sicknesses might inflate that number as well, if e.g. COVID alone or the flu alone wouldn't kill you, but both together are enough. Still, if deaths goes up by 10-20% seasonally you can figure that cases went up as well.
Having thought back through my comment, I'm not sure it makes sense. If a person has, say, the flu AND covid, AND has symptoms of one of them, AND tested positive for covid, it would be difficult to argue that this person ACTUALLY had a symptomatic flu case (unconfirmed by lab results) but an asymptomatic covid case (despite confirmation of covid infection by lab results). I suppose you could have a case where the person recovered from covid but still had some virus fragments detectable by PCR, and then caught the flu with active symptoms, but I doubt those types of cases are numerous enough to have the magnitude of effect I posited above....what do you think?
Just kidding. I think you are right still, because anything that sends you to the doctor is likely to increase the chance you are tested for COVID, so you are going to catch more cases whether they be asymptomatic or not. In the season for pesky bugs with COVID like symptoms that is probably more likely.
However, I do remember hearing, I think from Ivor Cummings, that COVID had supplanted the normal flu in the UK, and from other random medical sciencey sources that the various corona viruses compete against each other and periodically chase each other out of niches. So it might be that COVID detection isn't being helped by cold/flu seasonality because people aren't getting colds and flu, but COVID instead, which happens to share the same seasonality as other corona viruses. I don't know anything about how much COVID has replaced other strains of upper raspatory infections in the US, though.
This hypothesis (that seasonality results from a combination of temperature and herd immunity from previous infections) doesn't actually depend on immunity only lasting about a year. And indeed, most people don't get a flu every year, nor every kind of cold; more like once in 10 years.
Assume that the transmission rate is a product of a factor negatively correlated with temperature, and a factor positively correlated with how long ago you last had the same disease. At equilibrium, the long-term average of the transmission rate is 1. So, in temperate regions, r<1 in the summer, and r>1 in the winter (except if the current year's epidemic has already sufficiently increased the level of immunity to push r below 1—eyeballing the US flu death charts, they seem to peak in early January in the worst years, but later, in the spring, in years with low rates).
In this model, warmer regions should have less flu overall, since a longer interval between incidences corresponds to a long-term average r of 1. Maybe Alaskans get a flu, say, once in 8 years on average, Floridians every 12 years (still seasonally) and Panamans every 15 years (without seasonality).
>"In this model, warmer regions should have less flu overall, since a longer interval between incidences corresponds to a long-term average r of 1. Maybe Alaskans get a flu, say, once in 8 years on average, Floridians every 12 years (still seasonally) and Panamans every 15 years (without seasonality)."
I think I see the argument, but if so I think the argument's wrong? Here's what I think it was going for:
"For a disease at equilibrium, long-run average R=1. You can think of R=(transmission rate while infected)×(length of infection). So if transmission-rate-while-infected is lower in warmer climates, length-of-infection has to be longer, for the product to still be 1."
The fallacy there would be in switching out "time infected" (per infection) for "time between infections"; those would only be equal if everyone always got re-infected right after clearing the last one.
I didn't mean to consider the length of the infection; I assumed that it didn't depend on the weather. However, the time between infections affects the transmission rate while infected, because if people have got the disease a longer time ago, they have less immunity against it.
R = (transmission rate while infected) × (length of infection),
where (length of infection) is a constant, so (transmission rate while infected) also has to be a constant if R=1; and e.g.
(transmission rate while infected) = (sneeze rate) × (transmission prob. per sneeze)
where transmission prob per sneeze depends on how immune everyone else is; so e.g. in cold climates, infecteds sneeze more, but immunes are immune for longer, so in cold climates, infecteds' sneeze rate is higher but their transmission prob. per sneeze is lower*, such that (transmission rate while infected) is a constant, such that R=1?
---
*for whatever mechanistic reason, but if it wasn't true, then the pathogen either would have disappeared (R<1) or gone epidemic (R>1). (I wonder how equilibrium changes if there's migration; e.g. warm climates could be sources with local R>1, and cold climates could be sinks with local R<1, so that *global* average R=1.)
It's not that people are immune for longer in cold climates. It's that immunity wanes with time; in cold climates, people get a flu somewhat more often, so they have more immunity remaining from the last time they've caught it.
In my model, this is what creates an equilibrium: if a climate makes easier to transmit a disease for whatever reason, then people get it more often, that results in people having more immunity, which reduces r back to 1, i.e. equilibrium.
What do you mean by coming from warmer areas? And what do you mean by worse flus? Severity? Frequency of incidence? (Less frequent incidence could be compatible with more severe flus, if the lower frequency results in more waned immunity by the time you do catch it.)
How about it is actually humidity or cold but it should be averaged over a much bigger area, like North America or Europe where people interact sufficiently? Say the R of your virus depends slightly (say +-20%) on the average humidity/temperature over the region where people interact. Over the years, R has stabilized to be above 1 half of the year and below 1 the rest of the year (otherwise either the virus would be extinct or 99% of people would always have it). Then, the average humidity/cold/UV/whatever over a full continent tilts the R as we come into the winter and tilts it back in summer. Being in Florida does not protect you enough if there is enough people travelling back and forth with Alaska where the virus is thriving.
One piece of evidence that makes me thing that COVID seasonality is predominantly due to coldness/humidity is that meat processing plants were such fertile ground for the virus [0] [1]. These factories are basically building-size refrigerators, so they recreate the environment of winters.
Now, as you said, it can't be because of absolute coldness/humidity, because Alaskan summer is colder than Floridian winter, so it has to be relative coldness/humidity. (The meat factory workers presumably go to their warm homes after work, so they can never fully get used to the cold.) As your post on hypothermia death showed, humans are pretty sensitive to relative changes.
There was some speculation that masks work because they make the nose warmer [2]. If we turn this around, this means that a cold nose makes you more susceptible to catching COVID. Maybe people in colder climates are usually adapted to it and their body can keep their nose warm, but in winter, noses get a bit too cold. And similarly in warmer climates, the body usually doesn't have to keep the nose warm, so when it suddenly gets (even just a bit) colder, the nose gets colder and people catch diseases.
Meat packing plants are also crowded and loud, which are probably quite strongly correlated with COVID transmissions, which weakens (but does not eliminate) the evidentiary value of this observation.
Do we have a population spending lots of time in cold, quiet, lonely(ish, but not wholly isolated) places for comparison?
Growing up in northern England, even as a child I noted when playing outside in the snow you would get horribly cold, your feet would get numb, your ears would be frozen, and your nose would be runny, and then you would go indoors and have a hot bath or sit by the fire and let your wet cold feet thaw out. I wonder if the changes in body temperature somehow reduce immunity or increase vulnerability.
> The coronavirus seemed seasonal last year, but it was already everywhere, and there were no new strains (last winter was before the variants mattered much).
Just because they weren't given greek letters doesn't mean the 2020 variants weren't important. E.g., the G614 mutation caused a huge spike in cases worldwide in March 2020.
The spike in March 2020 was just initial introduction of the virus. It’s not like every region already had the classic version but waited for the new variant to have a spike - they all had spikes as soon as local transmission got established.
I believe this is correct. The epidemiology is in some kind of equilibrium: collective immunity and ease of transfer play role, both changing in time (collective immunity is downward sloping function of "time from the last peak", ease of transfer is function of year season). You need nothing more than this for the system to start to oscillate and get into a kind of resonance. It might be easily modelled I am sure.
The most destructive wildfires, or crown-fires, are uncommon under natural circumstances, when the much less destructive ground-fires predominate. Crown-fires do however happen often in actively-managed (or mismanaged) forests, where clueless or ideologically driven forest service suppress fires for decades, which leads to abnormal accumulation of deadfall (fallen branches, trees lying on the ground), and eventually there is so much of this dead dry mass that a randomly started fire becomes too hot to suppress and it destroys everything, down to the root.
Covidiocy manifesting as lockdowns and masking has so many similarities to the policy of fire suppression. Smart, evidence-based medicine, like vaccinations and targeted quarantines of select vulnerable populations, is very much like scientific forest management, with its prescribed burns.
I bet the differences in efficacy, measured in dead trees or dead people, will be similar.
At the start of the pandemic the rhetoric in favour of lockdowns wasn't so much about lowering the total number of cases, but about 'flattening the curve'.
Ie in your forest fire analogy, it would be acknowledging that since it's a new virus, by default every human is deadfall. So we need to burn through that accumulated dry mass in a controlled way (to avoid overloading the medical system all at once).
I want to make no judgement here on whether that was a good idea or not, just pointing out that some of the early rhetoric was pretty close to what you are describing.
Indeed, when confronted with a potentially massively deadly new and poorly characterized infectious threat it may be reasonable for individual citizens to voluntarily limit social interactions until sufficient information is available, and to avoid overloading the healthcare system. Unfortunately, the Covid lockdowns soon became politicized and being forced from above were not subject to the feedback loops that make voluntary interactions socially efficient. The net effect was trillions of dollars of economic losses, widespread emotional trauma and no lives saved to show for it.
You don't even need to go so far as saying no lives saved. That might be a bit controversial.
You can get a pretty interesting argument by just taking official or mainstream estimates of how many lives were saved and compare them with some reasonable estimates for costs of lockdowns.
If you can get enough data for an estimate, you should use QALYs instead of lives.
(It's a better idea in general, but also allows you to optionally give the lockdowns a cost in terms of quality of life.
Even if life under lockdown only costs something like 1% of quality of life for the duration, it quickly becomes damning, because everyone pays for it.)
> Can we use our improved understanding of disease seasonality against it? (...) At best, it would just put us in the same position as the tropics, where there’s nothing to constrain the disease’s rhythm, and it just strikes randomly.
Arguably, the most important point about corona pandemic is to prevent its spikes. I don't want to downplay the effects of the disease on individuals. (Deaths! Long covid!) But *the* reason for government intervention and lockdowns is the threat that our health systems might get overwhelmed.
For seasonal diseases (and perhaps even now for covid), the tropics are in a much better position because the spikes are smaller. That makes it a lot easier to deal with. It's like for transportation: our roads and public transport must be able to handle rush hours. If we could re-distribute that traffic evenly over the day, we could easily cut down our traffic infrastructure by half.
The total area under the curve is also important. Ie how many QALYs (quality adjusted life years) do we lose in total.
Interventions and treatments should be weighed and compared by how much they cost per QALY rescued.
You can integrate the concern about peaks into the general QALY framework. As you already point out, sizing a system to deal with peaks and troughs either is really expensive or insufficient.
How do we know that some diseases that appear seasonal aren't some complex, multi-year dance between communicable pathogens and the collective human immune system (that just happen to coordinate on emergence seasonally, but it's pretty much a distinct cohort each year)?
I definitely don't get the flu every year. More like every 7 years or so. Something something prime numbers....
"Yet I have never heard anyone claim that any winter diseases happen in summer in Arizona or Saudi Arabia or terrible places like that."
That made me curious as to what 'summer diseases' might be circulating in Saudi Arabia (indeed, are there such things as 'summer diseases'?) The closest I came to it was this:
(1) Study titled "Temporal trends in the incidence and demographics of cancers, communicable diseases, and non-communicable diseases in Saudi Arabia over the last decade" https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6468216/ - summation: vaccination programmes are knocking the usual illnesses (measles, smallpox, etc.) on the head, but as Saudi Arabia got richer, the population developed the diseases of affluence (diabetes, obesity, cardiovascular problems).
The incidental line that intrigued me was this -
"Cases of some infectious diseases were recently identified in Saudi Arabia, indicating that despite technological developments in diagnostics, treatment, and vaccination programs, various infectious diseases have re-emerged in Saudi Arabia after a decade. For instance, the prevalence of Middle East respiratory syndrome coronavirus infection increased in Saudi Arabia during 2012, and this disease continues to be a concern during the summer season and religious congregations in holy sites."
Okay! What looks like a summer disease! So that led me on to this:
Conclusion: First it *looked* as if there were seasonal peaks, but um, probably not. Also, it has to do with camels.
"Based on the occurrence of initial clusters in April 2012, April–May 2013, and May 2014, it was concluded that there was a significant MERS-CoV activity in March–May of each year. Initial hospital outbreaks also occurred in April 2012 (Zarqa public health hospital, Jordan), April–May 2013 (Al-Hasa Outbreak) and April–May 2014 (Jeddah outbreak). Thus, it was thought that MERS-CoV occurs predominantly during the spring (March–May). The occurrence of cases in the spring raises the possibility of seasonal cycles of MERS-CoV as camels give birth in March (spring) and MERS-CoV occurs commonly in young camels. Seasonal variation may reflect the risk of transmission of MERS-CoV between animals and humans.
...Seasonal variations among the transmission of respiratory viruses reflect the risk of animal-human transmission, difference in the circulating viruses, and the natural reservoirs of specific viruses [4]. Since the emergence of MERS-CoV, it was though that MERS-CoV transmission occurs through two seasons: the spring (March–May) and the fall (September-November). Seasonal variation may occur due to dromedaries’ calving season (November and March). In one study, the prevalence of MERS-CoV was higher among camels in the winter time (71.5%) than the summer time (6.2%).
In an analysis of MERS-CoV cases from June 2012 to July 2016, authors estimated mean monthly data for all the included studies and showed that MERS-CoV may have two peaks in the winter and summer months. However, we showed no definite seasonal variation of primary MERS-CoV cases despite initial peak in February and August 2015 and in March 2017."
So in conclusion - well, I'm not entirely sure what to conclude. A very scanty, cursory look doesn't seem to turn up summer diseases comparable to winter diseases, so the question still remains: why winter peaks?
I'd suggest taking out that 'whatever' about African-Americans getting flu more before someone quotes it out of context as you not caring about the greater rate (obv not what was intended).
"July in Alaska doesn’t have to outrun January in Florida, it just has to outrun January in Alaska, for the dubious honor of when Alaska’s destined-to-be-once-a-year flu season is going to be."
I think this is backwards (July in Alaska is not Alaska's flu season).
I think it should be "*January in Florida* doesn't have to outrun *July in Alaska*, it just has to outrun *July in Florida* for the dubious honor of when *Florida's* destined-to-be-once-a-year flu season is going to be."
(or alternatively "July in Alaska doesn’t have to outrun January in Florida, it just has to outrun January in Alaska, for the *genuine* honor of when Alaska’s destined-to-be-once-a-year *relatively flu-free* season is going to be", but that's a bit more awkward)
That was what I was getting at with my somewhat awkward "Alternatively..." rephrasing.
Maybe it's just me, but if "outrunning" is in a contest to *not* get the flu, then it's not "for the dubious honor of when Alaska’s destined-to-be-once-a-year flu season is going to be". The metaphor seems to switch direction halfway through the sentence.
Keep in mind that different pathogens 'prefer' different things.
Most viruses pretty much have to go from one human directly to another. Lower humidity might allow virus laden droplets to stay in the air for longer, but we are typically talking about minutes here.
In contrast, lice work rather differently. Or worms. Many bacteria have spores. Etc.
OK I've been saying that being vaccinated, I would like to get a small dose of covid. Is there something wrong with this? The whole 'narrative' that everyone must get vaccinated seems to be distorting everything... but I just don't know.
Yeah, I'm not actively trying to get sick, but covid is rampid (?ravid, sp, all over the place) where I live, (Wyoming county, NY.) Many of the people I'm working with have had it... so I'm just hoping for a little dose. Talking with people at a bar. (I'm working in the kitchen.)
If natural immunity is X times better than vaccine (X>1) then everyone doesn't need a vaccine, only those who haven't had it.
Before we had vaccines, some economists' blogs were speculating about the costs and benefits of giving large swaths of volunteers herd immunity in something like this way.
This is especially tempting, since young healthy people typically get asymptomatic or mild cases, but still suffer from lockdowns just the same.
I will say from experience having lived in both a very cold climate (northern Germany) and a very warm one (Florida), the human body adjusts its setpoints w.r.t. "this is cold" and "this is warm" to its environment: when I moved from Germany to FL, it was January, and I went swimming in the hotel pool because 50°F felt so warm. Is it possible that the thing that matters for disease vulnerability is not absolute temperature, but rather differences in temperature between the warm and cold seasons? Note that I'm not necessarily suggesting that the intensity of the disease cycle is proportional to the magnitude of this difference - simply that there's some threshold temperature difference between seasons above which disease dynamics are governed by that cycle. This would explain why the tropics, which have almost no such difference, have random disease cycles.
Even though some people have made related points, it gives a lot of insight to make a (simple) calculation with numbers in a very simple infection model.
The reproduction value R is the product of two factors:
- An intrinsic value R_0: how many people an average person infects in a population without immunity.
- A dynamic factor x: what percentage of people are currently susceptible (not immune).
Then R = R_0 *x. We all know now that an epidemic spreads when R>1, and does not spread if R<1.
Without seasons, R_0 remains constant, and R stays at equilibrium, R=1. On each day a few people lose their immunity. Let's say that immunity lasts for 200 days, then roughly 1/200 = 0.5% of the population become newly susceptible each day. This means that x increases by 0.5 percent points, and so R increases as well:
R = R_0 * (x_old + 0.5%) > 1 .
So the infection spreads, but not for long. As soon as 0.5 percent of the population have caught the disease, x goes down to its original value. Then R=1, and the system is back to equilibrium. This basically happens every day.
But what happens if we have seasons? This is a relatively sudden event that increases R_0. Let's say R_0 suddenly goes up by 10%, so by a factor of 1.1. Then R becomes
R = R_0_old*1.1 * x > 1.
So the infection spreads, and it spreads until x has decreased by a factor of 1.1. That is the case when roughly 10% of the susceptible people have been infected. So there is potential for a sudden surge of diseases, so a wave.
The point is that this is pretty independent of whether you live in Alaska or Arizona, even if they have very different base values of R_0. If R_0 suddenly increases by 10%, then ~10% of susceptible people will catch it before equilibrium is reached again. The main difference is that if Alaska has a higher base value of R_0, then fewer people will be susceptible in equilibrium, so we would expect a slightly *less* strong wave. But not by much. Let's say Alaska has 20% higher base value of R_0 than Arizona, then it will have ~20% fewer susceptible people, and the Alaska wave will be lower by 20%. My point is that this is not much of a difference, even though the difference between Alaska and Arizona is huge in this scenario: it would mean that even the winter in Arizona would *still* be 10% better than the summer in Alaska.
It bothers me a bit that the size of the wave in this model is "only" 20-fold larger than in the model without seasons, but I am not at all sure about the numbers. In 200 days after infection, you have lost some of your immunity, but you are not back to baseline. For seasonality, it's estimated that corona has 20-30% higher R-value in winter. (Studies which only take data from Europe even get 40% or more, but the data is probably pretty confounded.) I am not sure how sudden this change is. Does a lot of this happen in just a week or two?
Another thing is that this is a very simplistic model. For example, populations are not homogeneous, mixing is a non-trivial thing, and there are non-negligible delays. I would guess that real-world waves tend to overshoot the theoretical equilibrium for various reasons.
If you haven't seen it, you might want to take a look at this article:
<i>Abstract
Viral respiratory diseases (VRDs), such as influenza and COVID-19, are thought to spread faster during winter than during summer. It has been previously argued that cold and dry conditions are more conducive to the transmission of VRDs than warm and humid climates, although this relationship appears restricted to temperate regions and the causal relationship is not well understood. The severe acute respiratory syndrome coronavirus 2 causing COVID-19 has emerged as a serious global public health problem after the first COVID-19 reports in Wuhan, China, in late 2019. It is still unclear whether this novel respiratory disease will ultimately prove to be a seasonal endemic disease. Here, we suggest that air drying capacity (ADC; an atmospheric state variable that controls the fate/evolution of the virus-laden droplets) and ultraviolet radiation (UV) are probable environmental determinants in shaping the transmission of COVID-19 at the seasonal time scale. These variables, unlike temperature and humidity, provide a physically based framework consistent with the apparent seasonal variability in COVID-19 and prevalent across a broad range of climates (e.g., Germany and India). Since this disease is known to be influenced by the compounding effect of social, biological, and environmental determinants, this study does not claim that these environmental determinants exclusively shape the seasonality of COVID-19. However, we argue that ADC and UV play a significant role in COVID-19 dynamics at the seasonal scale. These findings could help guide the development of a sound adaptation strategy against the pandemic over the coming seasons.</i>
One thing that is important to note is that you shouldn't trust CDC or WHO flu data. The CDC deliberately inflates flu data to encourage people to get the flu shot. They do this by including pneumonia deaths in flu deaths when they occur during "flu season". So, a lot of the seasonality of flu deaths comes from the CDC's method of counting them.
This is pretty shocking. I found another complaint against this policy, some sort of internal memo [1]. The author cites the NCHS death statistics from 2001 [2], pointing out that of 62,034 deaths from "pneumonia and influenza", "61,777 ... were attributed to pneumonia and 257 to flu". It seems unlikely that the flu led to pneumonia 100% of the time. The CDC explains that the reason deaths are lumped together is to correct the underreporting of flu on death certificates [3], but this seems like a massive overcorrection. I can't really see why the CDC would make such an obvious error if not to encourage people to get their flu shot, wash their hands, etc. as the article you cite suggests. This seems (as far as I can tell) to be a blatant misrepresentation of the facts, which is quite upsetting.
Hmm, I'm just wondering how many covid deaths are from people who get covid and then pneumonia? And yeah I have zero trust in what my government tells me... sad.
I would guess there are far fewer edge cases now that testing is easier and widely available. Based on the CDC document I linked above, it looks like it's up to individual doctors to decide how to report deaths associated with Covid. In order to make the case that there's serious over-reporting of Covid deaths going on, you'd have to find a compelling reason doctors/nurses would choose to over-report. Maybe more funding? Better health insurance payouts? I don't know, but I doubt it's a big problem anymore.
Okay, the data from 2015 paints a much less extreme picture. 5,251 influenza deaths and 51,811 pneumonia deaths [1]. This would suggest a big change in behavior in doctors/nurses filling out death certificates; they have become much more likely to report influenza as the underlying cause of death for a patient. The underreporting the CDC is complaining about seems to have gotten less severe. From what I’ve read about death certificates though, it seems like the flu could have a lot more deaths attributed to it than what would seem plausible. Perhaps the CDC is being dishonest, but I doubt they would have done so if they had more reliable statistics to report.
It also suggests that the professor you’re citing is being misleading. From what I’ve read about Covid, I would guess many older people, especially those with pre-existing respiratory conditions are quite vulnerable to the flu. Whether they die from the influenza virus (viraemia) or some other reaction to it (cardiac arrest, ARDS, etc.) is irrelevant. So his report that he has had no patients who died directly from the flu is not very meaningful.
It’s still crazy to me that so much of the scientific and policymaking world has no idea about the discrepancies in these statistics. It suggests that the CDC needs to rearrange its priorities in favor of telling the public the truth rather than what’s “good” for them.
The fact of the matter is that very few people ever receive laboratory tests for influenza relative to the number of people who report with symptoms consistent with influenza infection, which is why you often see reference to the term "influenza-like illness" during the flu season. The only way to try to recover the number of influenza-related deaths (which should include secondary pneumonias and other downstream complications, as you suggest) is to do so indirectly by combining what's known about the case mix and outcomes among those with confirmed influenza with outside information (e.g., death certificates, hospitalization rates). All that modeling obviously involves assumptions and the attendant uncertainty.
If you read the second paper cited on the CDC's page explaining how they calculate influenza burden (Rolfes et al.), you'll see they do report ranges that suggest considerable uncertainty in burden and death estimates. Speaking as someone who's worked a little on flu and other infectious diseases subject to similar limitations in data capture, I think it is less accurate to report deaths with lab-confirmed influenza as the only deaths due to influenza. You have to do modeling or statistical correction to at least partially account for the considerable shortcomings of surveillance data.
Yes, in temperate zones polio was seasonal with peak in summer/autumn. But it's not a respiratory virus, and it spreads via the fecal-oral route. I'd guess that swimming was the seasonality factor for polio.
Children are disease vectors. They haven't yet built up immunity to as many diseases as adults and they have terrible hygiene. I wonder if kids going back to school in the fall kick-starts the disease season, and it peaks a few months later after spreading through the community?
Obvious way to disprove this: look at countries that don't take summer vacations, or that take their extended school vacations during some other season.
Note that epidemological models are nonlinear so they can produce much more complex behaviours than a harmonic oscillator can when driven in this way. There's all sorts of bifurcations and chaos theory going on.
I was just reading about a (testable) hypothesis called Temperature Dependent Viral Tropism in a paper by Shaw Stewart and Bach. Here's a link (but, you know, search if this link gets nerfed).
Re: both cold winters and hot summers forcing people inside: perhaps so, but I cuddle with the people in my house a lot less during hot summers than cold winters.
I think 'forcing people inside' is just a simplified reference to all behavioral adaptations to cold seasons, which are manifold. Maybe winter coats that gets used constantly and never get washed are transmission vectors, maybe indoor heating is a better vector than indoor AC, maybe people indeed cuddle more when it's cold.
Not that I think this overturns the rest of the analysis or anything, but I think it's relevant as a 'reality has a surprising amount of detail' thing. You can't just dismiss the whole topic of cold weather behavioral adaptations because someone summarized it as 'people staying inside more' and that summary is disproveable.
If HxNy were the only flu strain, we would approach herd immunity within several years, even through a cold winter. So the flu continues to mutate into different strains to evade immunity, and one of the major unmentioned factors here is this strain churn, means a (in reality, a set of dozens of) different strains circulates through populations each year. The consistent cyclicality of flu season is largely driven by strain churn, but that still doesn't explain the peak/trough and their correlation to seasons.
I'd speculate summer as the selection bottleneck in highly seasonal regions, and winter as the exponential part of infection S-curve. So: it's summer is northern Eurasia, and the living is easy, except for the immuno-compromised. Which strain is best able to make it through the summer? This is largely driven by which strain does the immune system have the least memory of. And since the immuno-compromised are usually old, this is perfect for finding something most other people have never been exposed to either.
Now it's September, and the flu has just faced a 99% mass extinction event - especially around the previous year's strain where R0 is approaching less than one. Whichever funky new (so old, it's new) strain was able to hang on and continue to infect is going to well poised to spread through the rest of the population. Through travel, hajj's, agrarian laborers etc, these selected for strains again move throughout the world causing another peak. Immunity to the new strain builds, and then we do the summer selection process all over again.
> Yet I have never heard anyone claim that any winter diseases happen in summer in Arizona or Saudi Arabia or terrible places like that.
No? I lived in a place like Arizona or Saudi Arabia, and if I remember correctly the consensus was that people always seemed to get sick when the weather changed; either from hot->cold or cold->hot.
Why is it so implausible that human beings themselves exhibit seasonality that nobody ever mentions it as a possibility? For most of human history, the differences in energy availability between summer and winter have been pretty large. Is it really that unlikely that we have vestigial evolutionary adaptations to reduce energy consumption during winter that could affect our immune systems?
Like: could it be that there is an evolutionary advantage to killing off the old and frail during the winter months when they would otherwise be diverting scarce nutritional resources from the young and healthy. Disease seasonality is a feature, not a bug.
I think one way to think about it is to consider the fact that the smallish seasonal advantages/disadvantages affect the reproduction number, which affects the number of cases logistically (in simple models). If R_0 is 0.9 for some virus in the summer and 1.1 in the winter, this does not mean that about 20% more people will be infected in the winter as compared to the summer.
Instead, it means that the virus will be dying out in the summer and grow exponentially at the beginning of winter.
For covid-19, it feels like R_0 is varying a lot more than 0.2 between the seasons. I mean, people are generally not stupid {{Citation needed}}. They might not be 100x as careful if the incidence is 100x as high as during summer, but they still will probably take additional measures sufficient to affect R to a measurable degree.
I am a bit confused about this temporary immunity thing. Evolutionary, memory cells make a lot of sense, which is why we have them, I guess. Is it just that having antibodies around allows for a quicker response, and that these tend to decrease over a few months?
Virus mutations will complicate matters, of course. Naively, I would expect the possibilities for mutation of a virus to be proportional to the number of infections. While recent viruses might travel between hemispheres twice a year, earlier ones were probably more at home in a single hemisphere? This would mean that the maximum proliferation of new variants coincides with maximum incidence. So to explain multiple waves, one would either have to assume mostly separate populations between which the virus can only travel occasionally or to assume temporary herd immunity again: 'Most mutations are created when infection rates are highest, but they initially can not spread far because of herd immunity. Only after herd immunity is decreased after a few months (or a year) can the mutations prove their merit by out-competing the other variants.'
Or it might be that hosts with a somewhat compromised immune system are not only the perfect places to stay during times of R<0, but also to acquire new mutations to evade existing immune responses.
I thiiink RJ, Brazil, is having a big flu outbreak now (I imagine it normally happens in winter? should check). Maybe the lack of a strong flu season in winter due to covid precautions screwed up the zeitegstgneber
my intuition is that you get seasonality under very broad assumptions (r0>1 and varies seasonally, immunity wanes on the order of at least a year) and the difference is made up by more people needing to get ill to get to herd immunity.
rt should be 1 on average in the long run
I think if we're comparing Alaska in the summer (rt<1) vs Florida in the winter (rt>1) the exponential growth/decay in cases should probably swamp the larger number of cases you'd get in Florida averaged over a year
someone should actually run the number here though
The tropics seem like they undermine this idea, but I want to get it out there:
Seasonality doesn't need to be caused by any external influence.
Consider cicadas. They have a normal seasonal profile of showing up during the weather they like, summer.
But there are also the 13-year and 17-year cicadas. They have a "seasonal" profile of spiking every 13 or 17 years. Nobody believes there's anything special about those years other than the surprisingly large number of cicadas coming out of the ground. Rather than an influence of the environment on the periodical cicadas, this is a special behavior of the cicadas.
There's no reason to believe a disease couldn't accomplish the same thing. Maybe diseases are seasonal because it's part of their life strategy.
That life strategy doesn't happen in a vacuum. So just calling it a life strategy doesn't anwer the question, it just gives the eventual answer a name.
From what I've heard, cicadas have to deal with predators, and that drives their prime numbered cycles.
For diseases, they have to deal with all the factors mentioned in the article.
> From what I've heard, cicadas have to deal with predators, and that drives their prime numbered cycles.
This isn't a real objection. Everything has to deal with predators. The predators have zero explanatory power for why the cycles happen in some cicadas.
They also have zero explanatory power for *how* the cycles happen in cicadas. And while you seem to want to talk about why the cycles happen, the topic of the post is how.
> So just calling it a life strategy doesn't anwer the question, it just gives the eventual answer a name.
Calling periodic behavior a life strategy answers the question of why it's happening. ("Because the organism is designed to do things that way.") This is conceptually separate from why doing things that way might be advantageous to the organism (Maybe it isn't! Warblers feed cuckoos because their design includes behavior that causes them to do that, despite the fact that feeding cuckoos is hugely disadvantageous.), and from how the behavior occurs.
I'm here to point out that the post above us is implicitly but very strongly committed to the idea that the cause of disease seasonality is to be found in environmental conditions, and this assumption is not actually warranted. Seasonality could be a behavior that the disease coordinates itself. In other words, the post is committed to an idea of *how* seasonality occurs that I believe bears further critical examination. The cicadas are an example of seasonality occuring without any reference to local environmental conditions. If cicadas can do it, diseases can do it to.
Why not have the greater infections during the winter be not a result of anything to do with the virus itself, but be determined by an intrinsic seasonal adjustment of the human immune system? That way it would be independent of the place because the people living in that place would come to recognize "winter" and "summer" and configure their immune systems accordingly.
Testable prediction of this theory: This means that someone who moved from one place to another might trick their immune system into being confused about what season it is and they would then be "out of sync" and thus more/less susceptible to viruses than the rest of the people living in the area who have been living there for a long time.
Your prediction can be broadened to include travelers. Especially when you compare travelers within hemisphere to those crossing the equator. (So that you can largely eliminate the influence of travel by itself as a factor.)
Slight complication: it's hard to observe the state of the immune system directly. And observing whether someone catches a cold or not, depends on whether a cold is going around just as much as the stand of their immune system.
1. Flu vaccines don't work well enough to explain the difference in influenza rates that black people experience.
2. COVID vaccines reduce hospitalizations and deaths but do not reduce case rates in any substantial way.
3. Neither of the above should be confused with other vaccines like, for example, MMR (measles mumps rubella) which are extremely effective and provide sterilizing immunity for years.
This is a very interesting take on COVID, influenza, and seasonality:
Do the flue vaccines not work so well, because there are so many strains (and the guess about what to vaccinate against is typically slightly wrong)? Or is the reason that they don't work so well in general, even when the guess is perfect?
PS The BCG vaccine is very interesting. Depending on country, it sometimes seems to provide no protection at all against the disease it's meant for, but it still lowers total mortality.
In South East Asia, we have two flu seasons a year - a summer season and a winter season - for EXACTLY the reason you mention - in the summer, people coop themselves up at home with the air-conditioning on full blast.
In the west, shade is adequate to cool you in the summer, so you don't need to close the windows and turn on the A/C. In South East Asia, the muggy air retains heat, requiring air-conditioning and reduced airflow.
Why doesn't that affect the United States east coast? The Bay Area has dry heat, as does the rest of the North American Pacific coast (though I'm not sure about Baja California, being a penisula), but even the cold parts of the eastern US have very muggy summers. Closing all the windows and shades is sometimes sufficient in the colder parts, but anywhere from Maryland south it is not, A/C is mandatory. This also applies to most of the Gulf Coast states - everywhere east of Texas, and some parts of Texas.
The vast majority of the population in SE Asia doesn't have in-home air conditioning. They have windows and fans. While they would *like* to close themselves up in an air conditioned sealed house, we just don't live in a reality where that is possible for anyone but the wealthy.
There are some countries where AC is more common like Singapore and Taiwan, but their populations are absolutely tiny compared to the populations of Philippines and Thailand.
Scott, have you seen the Temperature-Dependent Viral Tropism hypothesis, or TDVT?
The basic claim is that viruses evolve to thrive at temperatures below body temperature, to avoid infecting vital organs, to maximize host longevity and mobility, to maximize transmission and reproduction.
Also keep in mind that running an immune system is expensive and even somewhat risky. And the right alert level for your immune system is a result of many trade-offs.
Your idea of acclimatization would suggest that human immune systems' might also run on different settings in different places.
The entrainment / waning immunity mechanism can't explain chickenpox seasonality, since people generally don't get chickenpox (primary VZV infection) twice. So something else must be going on.
I think the overall idea is plausible but might not apply to all diseases.
New people are born who are vulnerable. Eventually there are enough of them that you get a burst of infections until their numbers are reduced. That burst happens in winter because reasons above.
Hmm, good point. I hadn't considered that.
The school year seems like the most likely suspect for chickenpox seasonality. The overwhelming majority of adults are already immune to chickenpox, so most of the vulnerable population is mostly school-age children. Schools provide a prime ground for chickenpox to spread, with large numbers of low-chickenpox-immunity demographics spending 30-ish hours a week cooped up in close contact with one another.
If chickenpox mainly spreads at school, then we'd expect a spike and fade at some point during the school year as it starts circulating at high levels and then burns itself out. Then it fades even lower starting in May/June when the schools close for the summer. Then in September, schools start up again with a fresh cohort of kindergartners joining the population. It would presumably take some time for residual cases to multiply into a spike, triggering the cycle once more.
Don't most people get chickenpox younger than that? I know I got it before I was in school.
I got chickenpox during elementary school years. My younger sister caught it in preschool, though. But that only gives a sample size of three.
I looked it up, and it seems like as of 2006 (when the vaccine was available but still ramping up in adoption), the peak age cohort for chickenpox infection was 5-9 years old.
https://www.researchgate.net/figure/Reported-varicella-incidence-by-age-group-United-States-2005-2006-compared-with_fig2_307577077
That might be the driver for other seasonal diseases too. I know I never got sick nearly so often as I did after I had kids in school. I wonder if you can find somewhere that the school year isn't synched up with the flu season.
In Japan school year starts in April. Nevertheless the influenza season is in winter between December and April.
But chickenpox infections in Japan do in fact seem to have two peaks, one in Spring, according to this study:
https://www.cambridge.org/core/journals/epidemiology-and-infection/article/role-of-temperature-in-reported-chickenpox-cases-from-2000-to-2011-in-japan/2F352DC1C7BAA94DD8ADD3E8C9B369F6
"In Figure 5, the LSF curves for all prefectures except Okinawa (Fig. 5h ) demonstrated a bimodal seasonal cycle with a first peak in winter (December–February) and a second peak in spring (April–June)."
So the start of the school year does not explain Okinawa. Also, according to this study, Canda has also the peak in Spring, not Winter. The study obove explains the two peaks with temperature.
Well, to be fair, the school year starts in April, then they have August off, then starts back up in September till July. So Japan has school year round, save for one month. Only the official year starts in April.
That does throw a wrench in the notion that it is all primary/secondary school driving things, however. College matches the western winter norm, but I doubt there are enough college students to drive things as effectively as school aged kids.
Yeah, I'd expect K-12 schools, especially elementary schools, to have a much bigger effect than colleges, for three reasons:
1. Younger children would be more immunologically naïve than college students.
2. Young children tend to be notoriously slapdash about the kinds of hygiene that reduce the risk of contagion, at least for diseases spread through fomites, droplets, and casual contact.
3. School-age children tend to live with their parents and (for younger children) have a ton of close casual contact with them, allowing a nice wide avenue for diseases to spread into and out of the adult community. Whereas college students tend to be much more sequestered in their respective campus communities, often living, dining, and doing most of their social activities either on campus or in nearby establishments that specifically cater to college students.
Anecdotal, but in the childcare services I work at, that's how it goes. New year starts in September, so heading right into the autumn/winter season. Colds go through everyone, including the staff, because if one kid gets it, everyone gets it. Ditto with other infectious diseases, so that's why we have a policy on "if the kid gets sick while attending, the parents are called to pick them up; if they get sick at home, they can't come in for 48 hours (until we know if it's communicable/they've stopped throwing up and pooping)".
"cooped up" --> I see what you did there.
Not sure how anyone would know at this point, but what's a seasonal COVID world look like? Are we talking death counts like 1) seasonal coronaviruses 2) RSVs 3) Influenza 4) Worse?
Assuming the two new pills work as reported, they drop the death rate by about an order of magnitude. So does vaccination or natural immunity from getting the disease. Combine those and the death rate is down by about two orders of magnitude, which I think gets it to or below the death rate from flu.
Do the new pills work specifically against Covid, or against all RNA viruses? Because if it's the latter, they could also reduce flu mortality by an order of magnitude.
Paxlovid is COVID-specific. Not sure about molnupiravir
Quoth Wikipedia: "Molnupiravir was originally developed to treat influenza at Emory University by the university's drug innovation company, Drug Innovation Ventures at Emory (DRIVE), but was reportedly abandoned for mutagenicity concerns."
Since the pills have to be taken early in the course of the disease (and generally before symptoms are bad enough to be scary) real world population effectiveness will depend on things like how likely people are to test, how easy it is to get from a test to a prescription in three days, compliance with the course (currently something like 40 pills in five days, though that often gets better as drugs are improved), etc.
My sense is that it will help quite a bit, but, especially in a world where there's a lot of disagreement about how serious Covid is to begin with, a lot of people won't bother with it until it's too late. (Or will find closing the test to pills in hand loop too slow, especially if they're not fast off the dime to get tested, or test results are slow to come back.)
I think that is where the efficacy will fall down - you have to take the new pills early. But how can you be sure that you have contracted Covid, rather than a cold? And testing is backed up because of the sheer numbers of people all wanting to get tested plus officialdom not accepting "I used a test kit I bought in the supermarket".
So you could have people panicking and running to the doctor for the new pill when it really is only a cold, and people waiting until the symptoms do get worse by which time the intervention is less effective.
It will be coordinated with the pharmacy. You won't need doctor's prescription as pharmacists in many countries are increasingly given power to assess the patient and provide prescription drugs. Ideally if you are symptomatic, you can get tested at the pharmacy and if positive, you can get your 5 day course of medicines there. Possibly even insurance paying for it, if you fulfil all criteria such as belonging to a risk group, of certain age, any comorbidities etc.
*many countries, but not the US.
It includes the US. Pharmacists can already do vaccinations in the US and vaccines technically are classified as prescription only. The scheme to dispense Paxlovid is entirely planned in the US.
I'm not sure those multiply when combined (but yeah, it looks mortality will be pretty much under control)
Well, one clue is the age gradient that it attacks. I'm no virologist, but COVID looks more like the cold than the flu in how it treats younger demographics, so in its fully endemic form, you'd expect it to be more like a seasonal coronavirus than the flu. But I have no idea of course.
I don't think it's unreasonable to hope thar thanks to spillover of state of the art vaccines from Covid to flu and RSV, as well as cross-immunity between Covid and endemic coronaviruses, that the net risk of dying from any of those pathogens could drop significantly within the next decade.
According to ONS's regular survey in the UK, >97% now have antibodies in the age group 50+. This means, they're more or less in the endemic stage now. Their daily COVID mortality numbers since late August ranged from 1.5 per million to 2.5 per million. Annualized, this yields the range [540dpm, 900dpm]. Assuming similar numbers for the US, this would mean something like 150k to 300k extra deaths per year, every year. To put this in context, CDC estimates yearly flu mortality burden to be 10k-50k from 2010 to 2020. So looks in its endemic state, SARS-2 won't be "just another cold", nor "just another flu", but rather, a nasty nasty (~5x worse) flu noticeably burdening the well being of the public.
Peru is about to hit 0.7% population excess mortality, so they must be at comparably high seroprevalence as the UK—meaning they too are probably at the endemic stage. Their flu season is from May to September, so they're not in flu season. They're currently recording ~1 COVID deaths per million daily. So 365dpm per year. Given their young demographic structure, this comports with our back-of-the-napkin calculation for the UK.
I would expect the mortality to drop drastically over time as the most vulnerable people can die only once.
Historically, diseases like Syphilis and HIV have become much milder over time, too.
New vulnerable people are continually created though.
No idea about Syphilis but HIV did not become milder over time. We developed treatments for it. Of course, the same will be true for COVID, but who knows how effective that'll be overall.
Compare https://www.bbc.com/news/health-30254697
Google has lots more articles about HIV becoming milder.
You are right that treatment also improved. That's a separate issue.
It's true that the CDC estimate influenza burden at 10-50k. But the excess death toll of "flu season" is much higher than that, and on the order of 60-120k extra deaths every winter, depending on whether you use the summer or fall months for how many deaths there "should' be. The difference in the numbers is the causal of death. Many of the winter deaths are due to other non-influenza seasonal flu viruses or bacteria.
Also I agree with Matthias that a declining CFR is more likely than an unchanging or increasing CFR. That probably put the burden of covid much more inline with another "flu season", if not with influenza specifically.
For now, it's worth adding, that flu itself still hasn't returned to the US. And even weirder, from what I can see of preliminary CDC data the regular "flu season deaths"(the distinction being seasonal deaths that may or may not be influenza, specifically) have not returned either. In other words, if you take total deaths and subtract covid deaths, the usual seasonality in deaths has virtually disappeared since Jan 2021.
I don't know how long this unusual situation can continue, but for now it seems like covid is replacing seasonal flu deaths, and not adding to them.
> Many of the winter deaths are due to other non-influenza seasonal flu viruses or bacteria.
Yeah, Influenza Like Illnesses ("ILI"), and other endemic diseases.
> Also I agree with Matthias that a declining CFR is more likely than an unchanging or increasing CFR. That probably put the burden of covid much more inline with another "flu season", if not with influenza specifically.
I don't know about that. That reasoning strikes me as wishful thinking. After all, ILIs keep killing similar amounts of people every year: the dry tinder doesn't get exhausted.
> flu itself still hasn't returned
Yeah, that's very interesting. It would be very fortuitous if a class of pathogens went extinct as a happy side effect of NPIs. But I'm not counting on it, most of them will probably return in a couple of years max. But it will be fascinating to examine in what ways the cohort born in 2020-2021 are healthier than the general population. We'll possibly confirm pathogenic origins of some cryptically caused diseases, like type-I diabetes.
FWIW - Peru has had an unusually rough time with covid. (why: climate? living conditions? genetics? altitude? medical care?)
Their recorded mortality stats are way off the charts and 2x-4x all of their neighbors, which were also hard hit. Some of that may be they are much better at actually recording deaths. But it's worth cautioning that to some extent their worst-in-the-entire-world experience may not be extrapolate to the experience of other countries.
Peru switched to counting all excess deaths instead of just PCR confirmed ones, so they look horrendous compared to other countries where deaths are undercounted by 2-5x. Here are some known excess population fatality rates (calculated from official all cause mortality stats) as they stand currently:
Bulgaria 0.78%
Russia 0.67%
Peru 0.67%
N. Macedonia 0.6%
Serbia 0.59%
Lithuania 0.54%
Mexico 0.47%
Romania 0.46%
Keep in mind that Peru—having entered the endemic stage—is more less done with the pandemic, but many Eastern European countries are in the middle of their current waves.
Given that Mexico and Peru have similar age structures, 70% of Mexicans having been infected, and 100% of Peruvians having been infected is consistent with their 0.47% and 0.67% PFRs respectively. Similarly, South Africa's 0.39% PFR, and their pop pyramid means that they too must be close to 100% attack rate. So doesn't look to me like Peru is this egregious outlier: their outcome is entirely predicted from Levin et al.'s IFR(age) function under the assumption that almost 100% got infected.
If the confounding factors like temperature and UV are really just a small influence, I'd expect at least some diseases to start their cycle in the summer, just by chance. Yet basically all infectious deseases are peaking in winter.
Also, if the non-seasonality in the tropics is caused by import, we should see a similar cycle in other countries, since more people are travelling between the hemispheres than from either hemisphere to the equator (to be fair, that's just an educated guess on my part).
Lastly, the immunity cycle should not allow double peaks. While it might be possible that the immunity "expires" with an offset of half a year for half the population, it would be far harder to actually peak for the virus since half of it's targets are already immune. Due to these network effects, I'd expect a wider curve instead of a peak.
That theory looks good, but I think we're still missing some pieces.
Double peaks for flu come from the fact that there are many strains and while immunity to a given one might last for years you can be exposed to a completely different strain 6 months later if you're unlucky; I'm basing this off knowing that flu vaccines in the Southern hemisphere are based on which strains caused the most recent Northern winter flu spike, and occasionally miss entirely and do nothing at all against the dominant strain in the Southern winter spike, and extrapolating that years where that happens would seem very likely to cause a double-spike in the tropics.
>Also, if the non-seasonality in the tropics is caused by import, we should see a similar cycle in other countries, since more people are travelling between the hemispheres than from either hemisphere to the equator (to be fair, that's just an educated guess on my part)
Scott talked about the part of the article which discussed Australia (more specifically the Top End, ie Darwin and surrounds). Darwin is heavily touristy, so a pretty large fraction of the people there at any given time are coming from elsewhere in Australia, much larger than the fraction of people in any major temperate city who are coming from the opposite hemisphere.
There's some other details in that article that Scott glossed over though, it mentions different flu patterns in different tropical cities. Darwin usually has one peak but sometimes has two. Singapore has two peaks. Colombia has year-round flu transmission, and Fortaleza in Brazil usually has one peak.
This seems to line up with an import theory. Singapore has many visitors from both hemisphres. Darwin mostly gets visitors from the Southern hemisphere and fewer from the Northern. Fortaleza mostly gets visitors from the southern parts of Brazil, and Colombia doesn't get many visitors at all (for its size, relative to the other places mentioned).
https://www.science.org/content/article/why-do-dozens-diseases-wax-and-wane-seasons-and-will-covid-19
“ Except in the equatorial regions, respiratory syncytial virus (RSV) is a winter disease, Martinez wrote, but chickenpox favors the spring. Rotavirus peaks in December or January in the U.S. Southwest, but in April and May in the Northeast. Genital herpes surges all over the country in the spring and summer, whereas tetanus favors midsummer; gonorrhea takes off in the summer and fall, and pertussis has a higher incidence from June through October. Syphilis does well in winter in China, but typhoid fever spikes there in July. Hepatitis C peaks in winter in India but in spring or summer in Egypt, China, and Mexico. Dry seasons are linked to Guinea worm disease and Lassa fever in Nigeria and hepatitis A in Brazil.”
Hm, that's a good counter point. Thanks for the citation!
Genital herpes peaks in spring/summer because its an std and more people are going out and thus having hookups in spring summer. Typhoid fever is salmonella based which as to do with with harvest cyles as well as meat spoling.
The point is not all diseases have the exact same factors which lead to the same cycles, there are variations based on individual characteristics and vectors of transmission. I dont have an exact model for this, but I don't this invalidates the basic hypothesis necessarily.
I think what you're missing here is that complex system dynamics with strong positive feedback mechanisms -- and a viral disease has one heck of a positive FB mechanism -- *often* exhibit large oscillations. You have only to think about stop-and-go traffic on the freeway. Where do those stops and goes come from? They will often seem to have no rational relationship to events on or the structure of the road (although we will all instinctively attempt to assign one, e.g. it was that nogoodnik in the #1 lane with an extra 20 feet of space in front of him). But these things, like water hammer in pipes, or predator-prey oscillations, Ice Ages probably, derive from dynamic instabilities in the system's evolution, and *don't* require any large effect to start or pace them. Even very small perturbations are enough to trigger large oscillations, and even very small nudges are enough to pace them.
Our intuitions about the dynamics of complex systems are often mistaken. So we expect there to be a big reason for why a thunderstorm happens now instead of 4 hours later, or why stop-and-go traffic develops here instead of there -- and why big oscillations in disease diagnoses happen in this month instead of that. But there can easily not be. It can easily be an instability of the underlying dynamics, with triggering (or pacing) factors that seem wholly insufficient in magnitude.
I mostly agree, but when I see a noisy dynamical system that exhibits pretty regular oscillatory behavior, this suggests to me that it is being driven by something with a similar frequency to its characteristic frequency. And I guess I'm a little surprised that so many diseases have characteristic times for increasing susceptible population that you see this level of seasonality? Especially if the system is (seemingly) not being driven very strongly?
Well, the problem is that seasonality affects everything on Earth, pretty much. The natural world (temperature, humidity, sunlight), the biological world (growing cycle, reproductive cycles of animals and insects), and us (we clearly exhibit seasonal variations in health, fitness, mood). So it's not at all surprising that *if* there are going to oscillations arising from underlying chaotic dynamics, they are willy nilly going to end up with some kind of approximately seasonal time constant. How could they not? There isn't any other important time in the system.
Not driven very strongly is exactly what I'm getting at. Unstable dynamical systems don't *need* a strong driving force, they can amplify a teeny tiny driving force so you get results that seem wildly out of proportion. Another example that comes to mind is electronic oscillators, which fall almost immediately into their extreme oscillation modes following undetectably small fluctuations.
That's why I'm saying when Scott says "hmm this driving force doesn't seem sufficientg" he's falling prey to the assumption that the underlying dynamics are stable, which is where our intuition naturally takes us. But they may not be -- indeed, I'd be quite surprised if they were, given the existence of the strong positive feedback loop in infection (the more people are infected, the faster new people get infected). That seems like an almost classical example of a highly unstable dynamical system, and the surprise would be if it *didn't* exhibit wild oscillations.
Yeah, I get that dynamical systems will spontaneously start oscillating in response to tiny perturbations (laser oscillators are another example of this). But getting them to stay in phase with an external driver over many cycles typically means that either the driver is strong or it is acting at a frequency close to the characteristic frequency of the system.
I do not think that 1 year is the only relevant timescale for an epidemiological system. Doubling time for many diseases is ~1 week, human behavior and biology have cycles on the scales of 1 day, 1 week, and 1 month, and some vaccines apparently only need to be boosted once every 10 years.
To be clear, I am not saying that this is mysterious or the driver must be strong. It's plausible to me that the dynamics of human diseases are such that all you need to see strong seasonality is for a population to regain susceptibility on any scale between a few weeks and a year, plus a weak driving influence with a period of a year. I just don't think "dynamical systems do this all the time" gets you more than "your prior on seasonality should not be very low".
Yes of course the natural frequency belongs to the infected population. But surely it can't be a surprise that the human population has natural frequencies that correspond to the seasons, right? Many such reasons have already been identified (crowding, sunlight) and I'm sure you can think of many more (nutrition, fitness, sleep, mood and self-care, school schedules). It would in general be surprising if oscillations in any aspect of human health did *not* have frequency components near the seasonal swing. (We know both births and deaths do, for example).
Sure, any driver has to have a frequency component near the natural frequency, but since most fluctuation spectrums are broad, this requirement seems almost trivial to satisfy. I would have a hard time thinking of any source of low-level fluctuating impulses that had a narrow-band spectrum. Can you think of any?
Your final sentence is in the direction I'm arguing, I would just make it far stronger: the nature of complex dynamical system is such that your prior on there being a clearly identifiable driver with (1) intuitively satisfying magnitude, and (2) matching narrow-band spectrum should be approximately zero.
But then I'm an empiricist, not a rationalist, and my prior on most plausible hypotheses on complex systems is zero to several decimal places. I've been surprised by such systems far too many times in practice.
Was reading recently that the time of day that you get vaccinated might make a difference
> They will often seem to have no rational relationship to events on or the structure of the road (although we will all instinctively attempt to assign one, e.g. it was that nogoodnik in the #1 lane with an extra 20 feet of space in front of him).
Sure, but they also often totally have a rational relationship to the structure of the road -- a curve that's too tight for traffic to flow at its normal rate, a merge point, etc. Just like there's a traffic jam at the bend in the freeway every weekday at 5:00, we have flu spikes every winter.
Yes, those would be a different case. I'm talking about the apparently inexplicable stop-n-go business that happens in LA traffic pretty much all rush hour, along hundreds of miles of freeway, with no obvious relationship to the features of the road. But that's just one example, there's a vast cornucopia of unstable dynamic systems that develop wild oscillations from trivially small fluctuations.
Are there any natural cycles in the human body that could account for some seasonality? Could be akin to asking why we are tired at night.
Probably easier to ask if we see the same sort of seasonality in other animals?
Combining the two, could the seasonality of pollen just act as a stressor on immune systems such that we are just more susceptible?
I had the same thought. What if for example there is some remnant of winter hibernation in humans that we barely perceive, but has an effect on virus resistance. That would explain why the outbreaks happen in whatever people consider "winter", regardless of the specific weather.
Plenty of other diseases have summer peaks, like apparently polio and gonorrhea.
Any chance those are understood?
The many articles I've seen on this topic in the past year and a half have had many theories, but none of them include a clearly correct explanation. The point is just that an explanation of one that predicts that all should have the same season doesn't seem likely to be correct, but an explanation that allows some variance between diseases might be more plausible.
Polio spreads especially well through water, right? And more people swim when it's summer.
I'm not a biologist, but the human body could well have adapted to learn something like "no need to keep immunity for more than six months" if it was costly to keep it for longer.
I doubt this applies to T-cells, where keeping information is very cheap, but might apply to antibodies, which are expensive to maintain.
It could be. Monica Ghandi pointed out that if your blood hung on to all the antibodies it ever produced, it would turn into a thick paste.
https://wtop.com/coronavirus/2021/07/infectious-disease-expert-disagrees-with-pfizers-covid-19-vaccine-booster-push/
Could pathogens be affected by the moon? Maybe seasonal disease come and go like the tide?
I mean, moon phase corresponds to weak or strong tides in an incredibly strong way - I'd be shocked if "the tides are more aggressive" didn't increase drowning in those parts of the month?
That would explain a monthly cycle, which I don't think has ever been observed, not the yearly cycle.
Sickness waxes and wanes with the inconstant moon. There are (roughly) thirteen lunar months in the year. Thirteen is an unlucky number. This is why! 😁
“ I have never heard anyone claim that any winter diseases happen in summer in Arizona or Saudi Arabia or terrible places like that.”
We did indeed see delta surge in southern states at precisely the time when everybody was indoors with AC. Could’ve been coincidence, but we have heard of it.
Also, in 2020, the second Covid wave hit in summer in heavily air-conditioned states like Arizona, Texas, and Florida.
I mean, Delta is a pretty good explanation on its own. But I agree with Steve re: 2020.
The most obvious naive explanation to me seems that humans have some seasonal patterns in their biological activity - which would make sense for an animal evolved in non-equatorial regions - and those patterns affect immune system activity. Is there a straightforward reason why this explanation is so wrong it's not even worth considering?
Also, what about human adaptability? E.g., what if in whatever climate you live, your body is going to do just good enough job to maintain the right temperature (36.6 C or whatever) in your sinuses most of the year, but when the temperature is at the local minimum your sinuses temperature is going to drop somewhat, providing a comfortable environment for the virus. Local lows are below human body temperature pretty much everywhere, so this model would work everywhere, and the "slightly below the normal human body temperature" is independent of external temperature so we'll see about the same effects in every place with seasons. Is there anything obviously wrong with this model?
Why would your body have a program to make the immune system work less well at a certain time?
The body certainly adjusts its temperature on a moment-by-moment basis, but I don't know if there's evidence that it does some kind of weird long-term adjustment where it lets body temperature be colder whenever outside temperature is colder than its mean value.
>Why would your body have a program to make the immune system work less well at a certain time?
To save the energy during the [presumed] times of hunger in winter? One could counter by saying that it's stupid and body should regulate such things based on the actual availability of nutrients, but it's equally stupid that we get sleepy based on ten random external and metabolic cues and not just whenever we lie down and relax, yet here we are.
>The body certainly adjusts its temperature on a moment-by-moment basis
Right, and as far as I understand that includes adjusting the temperature down a notch when it's kinda cold. And even though for you living in the bay area "kinda cold" is +5C (outside) but for someone in Central Russia "kinda cold" is -25C, but in both cases the body adjusts just a bit and arrives to roughly the same lowered temperature. What I'm trying to articulate is basically "people tend to feel cold in the winter more often" (though I don't have any studies to quote on this one unfortunately).
When I said "hunger" I should've said "scarcity", winter means not only potentially lower supply of nutrients but also necessarily higher demand on them to maintain the body temperature.
My 10 seconds of thought answer: Would it make sense for your body to just plan on getting diseases every so often, to develop immunity, and synchronize it with times when you're mostly just sitting around anyway?
In our ancestral environment did we spend winter "just sitting around"?
Actually in our ancestral environment, did we have winter? Kenya is in the tropics. I don't know what its seasons are like.
What do we know about seasonality of viruses in other animals? I'm wondering about bats, famously disease-ridden mammals that, much like humans, spend their spare time hanging around in huge groups and sharing pathogens, and also conveniently live all over the world but rarely travel between hemispheres. Do their viruses have seasonality? If so it might help us eliminate some of the theories like "it's because people spend winter indoors".
Keep in mind that the weather in Africa (and the rest of the world) has changed quite a lot in the last few million years.
The Sahara used to be green. We have ice ages and warm ages, etc.
_Unless_ some of the diseases can kill you, why bother to fight any of them? _If_ some of the diseases can kill you, how does your body know that those are the ones to fight(vs. just practice on)?
If it doesn’t kill you, but makes you less effective at getting the things that keep you alive, you want to fight it. Maybe that’s a way for it to “kill you”, but it’s not usually what we mean.
I don't follow. The poster I was replying to(Meefburger) was suggesting that possibly the human body _occasionally_ allows (some?) viruses to invade, so as to provide "exercise." My point was that there does not appear to be a method to evaluate viruses for lethality at-the-front-door. Thus this system would be very problematic and unlikely to have evolved.
I think I missed that aspect of the dialectic!
This doesn't have to be an either/or system.
Helminthic therapy suggests that _not_ getting infected by worms can be bad for you. https://en.wikipedia.org/wiki/Helminthic_therapy
Basically, biology is such a mess, that organisms actively rely on their imperfections, because evolution doesn't have a way to tell which aspects of us are features and which are bugs.
My current understanding is that "exposure" can not cause you to get a cold, but it can very well turn a flu into pneumonia. Walking around in the cold with an active virus is usually an unwise thing to do, especially if you have other risk factors. It may be that cold is triggering a "short term" orientation in the body - we're making sure things keep working now, and we'll restart the immune system tonight when we're warm and cozy.
I can also easily imagine other reasons for the same interference. Maybe lower overall blood flow may mean lower overall communication between circulatory and lymphatic systems. Or cold interferes in a mechanical way with immune cells properly reaching the respiratory system.
But yeah, this doesn't affect the main point: disease is a non-linear system that needs only small nudges to fall into a seasonal pattern.
Relevant https://onlinelibrary.wiley.com/doi/10.1002/rmv.2241
This paper claims viruses adapt themselves to local temperature changes to maximize their chances of staying in the upper respiratory tract to maximize spreading.
The explanation I've always heard is that cold and wet both reduce our immune response because the body has to spend more energy dealing with the cold and wet. Many of us have heard our mother's say "don't play in the rain or you'll catch a cold."
On the other hand, my respiratory therapist wife has said that people are more vulnerable to respiratory infections in the winter because it's so dry that the protective mucous membranes in the airway dry out.
That is, because the air is so dry. (Which is certainly true; the absolute humidity is always lowest in the cold season.)
Mostly only if you turn up the heat. If you put on an extra sweater instead, it's not quite so bad.
That only helps the relative humidity, not the absolute humidity (which will certainly help your skin and hair not dry out as much.)
It won't help your respiratory system much though; your lungs are very efficient at heating air to body temperature, so the relative humidity in the lungs is only a function of absolute humidity.
> Why would your body have a program to make the immune system work less well at a certain time?
I'm not a biology/medical person, but in women I understand that your immune system is suppressed during part of the menstrual cycle to promote pregnancy. Is there any reason why it would be better getting pregnant in the winter? Speculating wildly, but something to do with food availability?
I agree that although it might be a complex system, biological factors probably play greater role than suggested in the post. For example there is research that suggests that being cold dampens the immune system to some degree (https://pubmed.ncbi.nlm.nih.gov/10066131/), but there are other effects, for example that heating dries out the mucous membrane and probably there could be other factors as well. I think the idea in the original post that the virus only need to outrun itself locally compared to the summer was on to something. When we are combining all these factors it becomes very likely hat the virus will thrive in the winter compared to the summer. Why would it do the hard work in summer if it can wait for the far more ideal conditions in the winter?
I mean, if I'm gonna start running a fever to fight off a disease, I'd rather it be at a time of year that's cold enough that I can shed the heat.
Could the difference be us rather than the pathogen? Maybe people are more vulnerable in the winter for some reason. If you look at mortality by month for the U.S., it's high in the winter, low in the summer.
I responded elsewhere with a similar thought. Folksy wisdom has said for years not to play in the rain, for fear of catching a cold. Obviously you're not going to catch a pathogen playing outside by yourself, but it's probably still true as related to weakening your response to pathogens you have already been exposed to.
Many pathogens do not require human transmission.
Viruses are pretty fragile. Somewhat simplified: you pretty much have to catch a fresh virus directly from a fellow human. Bacteria and worms etc can survive outside their preferred hosts for much longer.
(Of course, reality is more complicated.)
Perhaps with all the vegetation going dormant in the winter there is just poorer air quality?
That would explain Alaska, but not Florida or California.
I know I tend to get a runny nose in cold environments -- surely I can't be an exception in this ? Runny noses would contribute to the spread of seasonal viruses, IMO.
This is also consistent with what seems to me to be a strong tendency for seasonal viruses to set up camp in my nose
I'm quite sure this is a preventative measure to stop viruses from taking hold. Viruses already don't do well in warm air, and your nasal passages are the first thing to vasoconstrict in cold weather, meaning there's less warm blood going through and your airways are more vulnerable to infection. The runny nose tries to compensate for this by flushing them out instead.
I've personally noticed that, pre-pandemic, when I wear a scarf over my nose and mouth in cold weather, I'm drastically less likely to catch a cold. It's unlikely that a woollen knit scarf is stopping any viruses from getting through so I believe that letting the warmth of my breath circulate, instead of just escaping, is why it's harder to get sick.
> The runny nose tries to compensate for this by flushing them out instead.
It was counter-intuitive to me so it took me a long time to notice, but, yeah, when I am dehydrated my nose runs more. (My intuition would say that my body should be trying to save moisture when I'm dry.)
I don't have much knowledge on the subject but I'll toss out an idea that animals could have something to do with it, since there's a lot of animals that change their behaviors drastically based on seasons (mating, migration, etc.) Maybe some animals or insects develop some new disease variants over time, and seasonal behavior causes them to transmit it to humans. Though it would be disproved if a lot of these diseases don't originate from animal sources.
Animal reservoirs are important for some viruses, but when I looked up chickenpox, there are no corresponding animal/insect-to-human transmission. So that knocked that theory on the head for me, as chickenpox is apparently seasonal with most cases in winter/spring.
I dunno, maybe it has to do with when the stars are right!
Maybe more people swimming in salt water during the summer months kills off a lot of pathogens?
Then you'd expect a pretty strong coastal vs inland discrepancy in viral transmission, and I've never heard of such a thing.
And away from natural bodies of water, most swimming happens in chlorinated pools, I guess?
A few corrections on vitamin D:
1. No reason to choose this specific Australian study of the dozens of RCTs, just because it happens to be the most recent one. It's not like this is a constantly changing field.
This is a much better source: https://www.bmj.com/content/356/bmj.i6583
It's a meta-analysis covering 25 RCTs, and it finds a significant protective effect, including a very strong one for deficient individuals.
2. It's not surprising the Australian study wasn't successful, since: a) It used bolus doses, which the meta-analysis also found to be ineffective (interestingly, both studies got almost the exact same effect and CI!); and b) It was done in a sunny country. You can see that the vit D levels of the controls (77.5 nmol/L) was higher than any country in Europe (mostly 40-60): https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4288313/#b5025
3. Nevertheless, the Australian study still managed to reach significance on duration and severity.
4. Most importantly, it's wrong to extrapolate from the effect of vit D on the individual to the whole population. Even if we accept the wrong conclusion that an individual has only a slightly shorter duration and viral load, the multiplicative effect of that as the virus goes through the population (20-30 generations?) could be huge. For example, 0.95^25 is 4x.
My personal impression is that vitamin D and close unventilated spaces are the main factors (note that in summer there is usually better ventilation).
+1, my understanding has always been that the literature on vitamin D for reduction in seasonal illness is basically positive.
Indeed, and importantly the supposedly failed Australian study actually perfectly agrees with the meta-analysis.
May I be a bit lazy and ask you instead of digging through the sources? My current understanding is that vit D level is important, but for some (weird) reason it's much better if you got to that level by sun exposure than by (commonly available) supplements. Is that true?
I don't know of a study supporting that, but it makes perfect sense. Vit D metabolism is fairly complex, and supplementation may be missing something.
Additionally, sunlight is involved in other processes like releasing nitric oxide. Won't be surprising to discover there are other processes.
But putting a few drops in water is much easier than sitting in direct sunlight for an hour.
> for some reason it's much better if you got to that level by sun exposure
Do we even know *that*? It's a very plausible theory, but right now we have a lot of correlation and not much surety about causation.
It's just in my memory banks. Thiscis why I was looking for corroboration...
Trouble with Vitamin D supplement is you are supposed to take it with a fatty meal. I never know when the next fatty meal arrives and when it is there I'm all over it without thought of any pills.
It's not a must. According to this study it's just a 32% improvement.
https://pubmed.ncbi.nlm.nih.gov/25441954/
What about diseases with other seasonalities? https://www.sciencemag.org/news/2020/03/why-do-dozens-diseases-wax-and-wane-seasons-and-will-covid-19
E.g., chickenpox is spring seasonal. (And as Metacelsus mentioned, an immunity-based mechanism can't apply to it.) And other diseases have other seasonalities...
Another seasonal factor that could partly contribute to nudge a dynamic system in cycles is school terms.
The years I was most often sick with the flue were those with young kids at school.
Don't know if different school schedules near the equator would support this.
To make things slightly more complicated, not all seasonal viruses peak in winter. When the US suffered from annual polio epidemics in the first half of the 20th century, they would come in summer. I'm not sure why this is (or if anyone knows), although I think it was spread by water and one factor might have been swimming in shared pools.
This would fit with the theory given here if polio just happened to have some different relationship to heat, humidity, etc.
> I think maybe they’re saying something like that getting a virus like this usually gives you about a year’s worth of immunity before your immune system “forgets” it
Does anyone know why the human immune system will forget certain viruses in a year, but retain a strong immunity to certain other viruses for a whole lifetime?
Likely the immune reaction is somewhat similar but the viral growth rate inside the host could be orders of magnitude different. (Difference is in the virus not the hosts reaction....)
There are different levels of your immune system. Your T-cells can remember forever at little cost, but those are kind of the last line of defense. (I'm not an immunologist or even a biologist.) Your active immune system is the first line and it seems like it needs some "exercise" every now and then to stay in proper working order.
Not only different levels, but entirely different aspects.
We have different 'parts' of the immune system for fighting worms (and other such parasites), viruses and bacteria. I don't know if there's an extra mechanism for fighting (pre-) cancer, but it wouldn't surprise me.
"If you came up with some multidimensional dryness-coolness-indoorness metric, then maybe places could be high on one or two in the summer, but the combined metric would always be highest in the winter everywhere.
This is possible. I just find it hard to believe that the place where this metric is highest in summer doesn’t even overlap with the place where the metric is lowest in winter."
I think seasonality can probably be explained by a combination of this multi-dimensional metric PLUS network effects and waxing and waning rhythms of immunity.
Network effects = Texas gets more winter infection because of spread from colder states in the North
Waxing and waning immunity = Texas gets more winter infection because immunity is high post winter / into summer months, but by the time the next winter rolls around immunity has waned. So there will be natural waves / a rhythm to infection.
I think this waxing-waning rhythm is why we're currently seeing an uptick in all non-COVID viruses. 18 months of lockdowns globally, suppressed non-COVID viruses (including gastro) to a much lower effective R and now that restrictions have eased, the effective R is higher than in a normal season. My paediatrician friend in the UK reports a severe several months of non-COVID viral infections post relaxation of lockdowns, particularly in children aged 18 months to 3 years, who have limited prior exposure (eg. a lot of deterioration of bronchiolitis). I've also seen a lot of severe bronchiolitis in my clinical work in Australia post-lockdown.
I also suspect more winter infection occurs due to resource-depleted individual immune systems - eg. kids from childcare (and their close contacts) get many viruses in a row in winter in part because immune responses are depleted by prior infections.
My guess is "sunlight deficiency" broadly. Modern humans are naturally sunlight deficient because we spend way more time inside than our ancestors did, and the deficiency is much worse when days are short — so we should expect things to go particularly wrong in winter.
In this model, disease susceptibility could be mediated by any number of factors: vitamin D, nitric oxide, circadian rhythms...
I'm also confused by Scott's argument against vitamin D. I mean his fourth point on Why Vitamin D Doesn't Work is literally, "Black people have less vitamin D and oh wait, they actually do catch the flu more often."
Also note re: Vitamin D, African-Americans are horribly vitamin D deficient and do/did catch COVID far more often and more seriously than whites. This part of the case feels really quite weak as a consequence.
Also note the case of Sweden. Much better outcomes than the rest of Europe, a fact that pro-lockdowners are constantly trying to obfuscate by refusing to look at data from outside of Scandinavian countries. They claim the Nords are some sort of alien race whose culture magically wards off COVID and cannot possibly be compared to anywhere else in Europe - presumably many of these people have never actually been to Sweden - so actually Sweden did badly. But their culture isn't actually the same, partly because Sweden has such disproportionately huge numbers of migrants from Africa. Who, guess what, are all horribly Vit D deficient compared to the Swedish population.
Overall I really didn't follow the argument as to why Vit D is so clearly the wrong answer. When you add back in the evidence that wasn't included, it does seem at least highly plausible.
Pretty sure his argument is mostly based on priors; vitamin D *notoriously* has false positives for helping with everything, so some positive results are expected regardless of whether its helpful (and should be discounted as evidence accordingly.)
When I think about this, I usually attribute it to holidays. I know its very US-centric to think of it this way, but you have Halloween followed by Thanksgiving followed by Christmas followed by New Years it comes out to a lot of times where people will travel to visit family and possibly spread diseases to new areas.
But I have all the medical skills of a wireless Xbox 360 controller, so I'm going to pretend its Vitamin D just like everything else.
Doesn't work because Australia still celebrates Christmas at the same time but gets their diseases in July.
Compare also timing of Muslim, Hindu and Chinese festivities.
Additional factors that might make people have weaker immunity in winter:
* fewer fresh fruits and vegetables available to eat
* less exercise
* exposure to cold temperatures weakening immune response by systemically raising cortisol levels and causing vasoconstriction that makes it harder for white blood cells to move around.
> fewer fresh fruits and vegetables available to eat
Is this a meaningful difference in rich countries in the 21st century?
Given the diets of first-worlders, it could well be that we're the worst off!
That would predict all viruses to have the same season but it looks like for every month, there is a virus with that month as it’s peak.
https://www.science.org/content/article/why-do-dozens-diseases-wax-and-wane-seasons-and-will-covid-19
I really recommend this paper:
Seasonality of Respiratory Viral Infections, Miyu Moriyama et al, Annual Review of Virology 2020
"The seasonal cycle of respiratory viral diseases has been widely recognized for thousands of years, as annual epidemics of the common cold and influenza disease hit the human population like clockwork in the winter season in temperate regions. Moreover, epidemics caused by viruses such as severe acute respiratory syndrome coronavirus (SARS-CoV) and the newly emerging SARS-CoV-2 occur during the winter months. The mechanisms underlying the seasonal nature of respiratory viral infections have been examined and debated for many years. The two major contributing factors are the changes in environmental parameters and human behavior. Studies have revealed the effect of temperature and humidity on respiratory virus stability and transmission rates. More recent research highlights the importance of the environmental factors, especially temperature and humidity, in modulating host intrinsic, innate, and adaptive immune responses to viral infections in the respiratory tract. Here we review evidence of how outdoor and indoor climates are linked to the seasonality of viral respiratory infections. We further discuss determinants of host response in the seasonality of respiratory viruses by highlighting recent studies in the field."
> Some people get the disease, it spreads exponentially until lots of people are immune, and then it stops until something changes.
Isn't it a problem for this theory that most people _don't_ get flu in any given flu season? In a typical flu season maybe 1% of the population gets flu, this isn't enough to meaningfully change the overall population immunity.
Possible counterpoint: most people do have some degree of flu immunity at any given time due to exposure to other strains. Each year you've only got a few percent of the population actually susceptible to getting flu; a wave of flu comes through and infects a third of those; now you're back to 98% immunity instead of 97% and that's enough to put the R below zero for another nine months or so.
Alternately, many people get the flu, but an asymptomatic case. Felt a little run down one Sunday? It wasn't a late night at the bar, but a minor case of flu. Regretting eating at Taco Bell? Flu, not food poisoning. Thought your kid picked up a bit of a cold at school? Bit of the flu. Etc.
Flu cases very rarely result in people actually going to the doctor and getting tested, even when they get a case bad enough to stay home from work or school. The CDC has (up till last year at least) given a range of flu deaths of +100% the official estimate, because frankly no one knows or bothered to check much to confirm what people died of if it seemed natural. If you don't wind up in front of a doctor who does the test, no one ever knows you had the disease.
The corona virus family is tricky like that.
Its 10% infected per year, so substantial chunk of vulnerable population. Hard to know what true R0 of flu is given people have some form of immunity, but Spanish flu averaged 1.8, so need 45% infected for herd immunity (estimated to actually have infected 35%). Given some people likely will still be immune after a year, 10% is a huge share of vulnerable population and likely create temporary herd immunity.
I think we need to say that at least 10% of the population are infected by flu; we don't know the upper limit because we don't test enough to know since many people who get infected don't know and don't get tested. We just know how many get tested and turn out positive out of the entire population.
You only need to test a representative sample. The size of that sample is independent of the size of the population.
The last sentence might seem counterintuitive, until you remember that you only need to sample your suspicious dice a finite number times, no matter how large or even infinite the potential number of times you could roll them is.
I don't know, if anyone is doing random sampling for flu prevalence testing.
I understand the statistics. What I am saying is that we don't randomly test people for the flu, we test people who go to the doctors and get tested, either because they have flu like symptoms or the office just tests everyone. So we do not have a representative sample, we have a very biased sample, only those who decide to go to the doctor and see if they have the flu. Our sample is dependent on both people getting the flu AND deciding to go get tested, where what we care about is how many people get the flu, regardless of whether they decide to get tested.
To put it another way, we have the survey problem. Say you want to find out how many people have jobs in a town. You go to the mall some Tuesday morning and interview the people there, asking "Are you employed?" You are going to get a biased sample, the answer probably biased downwards, because you are not getting a representative sample of the town people, but rather a sample of people who happen to be in the mall on a Tuesday morning. The people in the mall on a Tuesday morning are less likely to have jobs than the general population, because people who have jobs are more likely to be at them than at the mall.
Most of our medical testing for diseases that have wide ranges of symptom severity, and thus a wide range of people getting them checked at a doctor, suffer the same issues as surveys in general. We can't get a representative sample of the whole population without a great deal of expense and time. At least we don't have as much of a problem with social desirability bias as with regular surveys.
Are you sure that we don't test random people for the flu?
Yes, most people we test for the flu are not randomised, as your correctly point out.
But do you know that we don't have a small amount of proper randomised testing going on?
(The existence of the non random testing doesn't invalidate the randomised testing, as long as you don't mix up your numbers.)
Perhaps covid seasonality is somewhat dependent on the seasonality of other winter ailments like cold and flu. covid is just the one you get tested for most when you have cold- and flu-like symptoms. So maybe seasonality of other diseases causes more covid testing, which causes more covid positives "cases", the relative number of which is somewhat independent of the absolute level of covid infection in the population.
You know, I hadn't thought of that, but yea that would totally screw with using case counts as as estimate for actual cases. Damn, very clever! Where's the like button ...
I suppose you could mitigate that a bit by comparing deaths, but even then, all the seasonal sicknesses might inflate that number as well, if e.g. COVID alone or the flu alone wouldn't kill you, but both together are enough. Still, if deaths goes up by 10-20% seasonally you can figure that cases went up as well.
Having thought back through my comment, I'm not sure it makes sense. If a person has, say, the flu AND covid, AND has symptoms of one of them, AND tested positive for covid, it would be difficult to argue that this person ACTUALLY had a symptomatic flu case (unconfirmed by lab results) but an asymptomatic covid case (despite confirmation of covid infection by lab results). I suppose you could have a case where the person recovered from covid but still had some virus fragments detectable by PCR, and then caught the flu with active symptoms, but I doubt those types of cases are numerous enough to have the magnitude of effect I posited above....what do you think?
Does my approval fill you with shame? :P
Just kidding. I think you are right still, because anything that sends you to the doctor is likely to increase the chance you are tested for COVID, so you are going to catch more cases whether they be asymptomatic or not. In the season for pesky bugs with COVID like symptoms that is probably more likely.
However, I do remember hearing, I think from Ivor Cummings, that COVID had supplanted the normal flu in the UK, and from other random medical sciencey sources that the various corona viruses compete against each other and periodically chase each other out of niches. So it might be that COVID detection isn't being helped by cold/flu seasonality because people aren't getting colds and flu, but COVID instead, which happens to share the same seasonality as other corona viruses. I don't know anything about how much COVID has replaced other strains of upper raspatory infections in the US, though.
"The tropical parts of Australia are near the equator and don’t naturally have seasons"
Not true. There are two seasons in Darwin - the too hot, too humid, and too wet one, and the too hot, too humid, and slightly less wet one.
This hypothesis (that seasonality results from a combination of temperature and herd immunity from previous infections) doesn't actually depend on immunity only lasting about a year. And indeed, most people don't get a flu every year, nor every kind of cold; more like once in 10 years.
Assume that the transmission rate is a product of a factor negatively correlated with temperature, and a factor positively correlated with how long ago you last had the same disease. At equilibrium, the long-term average of the transmission rate is 1. So, in temperate regions, r<1 in the summer, and r>1 in the winter (except if the current year's epidemic has already sufficiently increased the level of immunity to push r below 1—eyeballing the US flu death charts, they seem to peak in early January in the worst years, but later, in the spring, in years with low rates).
In this model, warmer regions should have less flu overall, since a longer interval between incidences corresponds to a long-term average r of 1. Maybe Alaskans get a flu, say, once in 8 years on average, Floridians every 12 years (still seasonally) and Panamans every 15 years (without seasonality).
>"In this model, warmer regions should have less flu overall, since a longer interval between incidences corresponds to a long-term average r of 1. Maybe Alaskans get a flu, say, once in 8 years on average, Floridians every 12 years (still seasonally) and Panamans every 15 years (without seasonality)."
I think I see the argument, but if so I think the argument's wrong? Here's what I think it was going for:
"For a disease at equilibrium, long-run average R=1. You can think of R=(transmission rate while infected)×(length of infection). So if transmission-rate-while-infected is lower in warmer climates, length-of-infection has to be longer, for the product to still be 1."
The fallacy there would be in switching out "time infected" (per infection) for "time between infections"; those would only be equal if everyone always got re-infected right after clearing the last one.
I didn't mean to consider the length of the infection; I assumed that it didn't depend on the weather. However, the time between infections affects the transmission rate while infected, because if people have got the disease a longer time ago, they have less immunity against it.
Oh ok. So would it be something like
R = (transmission rate while infected) × (length of infection),
where (length of infection) is a constant, so (transmission rate while infected) also has to be a constant if R=1; and e.g.
(transmission rate while infected) = (sneeze rate) × (transmission prob. per sneeze)
where transmission prob per sneeze depends on how immune everyone else is; so e.g. in cold climates, infecteds sneeze more, but immunes are immune for longer, so in cold climates, infecteds' sneeze rate is higher but their transmission prob. per sneeze is lower*, such that (transmission rate while infected) is a constant, such that R=1?
---
*for whatever mechanistic reason, but if it wasn't true, then the pathogen either would have disappeared (R<1) or gone epidemic (R>1). (I wonder how equilibrium changes if there's migration; e.g. warm climates could be sources with local R>1, and cold climates could be sinks with local R<1, so that *global* average R=1.)
It's not that people are immune for longer in cold climates. It's that immunity wanes with time; in cold climates, people get a flu somewhat more often, so they have more immunity remaining from the last time they've caught it.
In my model, this is what creates an equilibrium: if a climate makes easier to transmit a disease for whatever reason, then people get it more often, that results in people having more immunity, which reduces r back to 1, i.e. equilibrium.
Given that flus come from warmer areas, and that warmer areas get worse flus, this would seem to be the opposite of reality.
What do you mean by coming from warmer areas? And what do you mean by worse flus? Severity? Frequency of incidence? (Less frequent incidence could be compatible with more severe flus, if the lower frequency results in more waned immunity by the time you do catch it.)
How about it is actually humidity or cold but it should be averaged over a much bigger area, like North America or Europe where people interact sufficiently? Say the R of your virus depends slightly (say +-20%) on the average humidity/temperature over the region where people interact. Over the years, R has stabilized to be above 1 half of the year and below 1 the rest of the year (otherwise either the virus would be extinct or 99% of people would always have it). Then, the average humidity/cold/UV/whatever over a full continent tilts the R as we come into the winter and tilts it back in summer. Being in Florida does not protect you enough if there is enough people travelling back and forth with Alaska where the virus is thriving.
One piece of evidence that makes me thing that COVID seasonality is predominantly due to coldness/humidity is that meat processing plants were such fertile ground for the virus [0] [1]. These factories are basically building-size refrigerators, so they recreate the environment of winters.
Now, as you said, it can't be because of absolute coldness/humidity, because Alaskan summer is colder than Floridian winter, so it has to be relative coldness/humidity. (The meat factory workers presumably go to their warm homes after work, so they can never fully get used to the cold.) As your post on hypothermia death showed, humans are pretty sensitive to relative changes.
There was some speculation that masks work because they make the nose warmer [2]. If we turn this around, this means that a cold nose makes you more susceptible to catching COVID. Maybe people in colder climates are usually adapted to it and their body can keep their nose warm, but in winter, noses get a bit too cold. And similarly in warmer climates, the body usually doesn't have to keep the nose warm, so when it suddenly gets (even just a bit) colder, the nose gets colder and people catch diseases.
[0]: https://www.news-medical.net/news/20210927/Irish-meat-processing-plant-COVID-19-outbreak-a-retrospective-study.aspx
[1]: https://www.business-humanrights.org/en/latest-news/germany-1500-workers-test-positive-for-covid-19-at-meat-processing-plant-company-criticised-for-failure-to-protect-workers/
[2]: https://twitter.com/diviacaroline/status/1378059132381523968
Meat packing plants are also crowded and loud, which are probably quite strongly correlated with COVID transmissions, which weakens (but does not eliminate) the evidentiary value of this observation.
Do we have a population spending lots of time in cold, quiet, lonely(ish, but not wholly isolated) places for comparison?
Growing up in northern England, even as a child I noted when playing outside in the snow you would get horribly cold, your feet would get numb, your ears would be frozen, and your nose would be runny, and then you would go indoors and have a hot bath or sit by the fire and let your wet cold feet thaw out. I wonder if the changes in body temperature somehow reduce immunity or increase vulnerability.
Compare https://en.wikipedia.org/wiki/Contrast_bath_therapy
Interestlingly, German Wikipedia https://de.wikipedia.org/wiki/Sauna#Medizinische_Wirkungen suggests that sauna (and cold shower afterwards) helps the immune system, but English Wikipedia doesn't mention that.
> The coronavirus seemed seasonal last year, but it was already everywhere, and there were no new strains (last winter was before the variants mattered much).
Just because they weren't given greek letters doesn't mean the 2020 variants weren't important. E.g., the G614 mutation caused a huge spike in cases worldwide in March 2020.
The spike in March 2020 was just initial introduction of the virus. It’s not like every region already had the classic version but waited for the new variant to have a spike - they all had spikes as soon as local transmission got established.
I believe this is correct. The epidemiology is in some kind of equilibrium: collective immunity and ease of transfer play role, both changing in time (collective immunity is downward sloping function of "time from the last peak", ease of transfer is function of year season). You need nothing more than this for the system to start to oscillate and get into a kind of resonance. It might be easily modelled I am sure.
The mention of wildfire is most apt:
The most destructive wildfires, or crown-fires, are uncommon under natural circumstances, when the much less destructive ground-fires predominate. Crown-fires do however happen often in actively-managed (or mismanaged) forests, where clueless or ideologically driven forest service suppress fires for decades, which leads to abnormal accumulation of deadfall (fallen branches, trees lying on the ground), and eventually there is so much of this dead dry mass that a randomly started fire becomes too hot to suppress and it destroys everything, down to the root.
Covidiocy manifesting as lockdowns and masking has so many similarities to the policy of fire suppression. Smart, evidence-based medicine, like vaccinations and targeted quarantines of select vulnerable populations, is very much like scientific forest management, with its prescribed burns.
I bet the differences in efficacy, measured in dead trees or dead people, will be similar.
At the start of the pandemic the rhetoric in favour of lockdowns wasn't so much about lowering the total number of cases, but about 'flattening the curve'.
Ie in your forest fire analogy, it would be acknowledging that since it's a new virus, by default every human is deadfall. So we need to burn through that accumulated dry mass in a controlled way (to avoid overloading the medical system all at once).
I want to make no judgement here on whether that was a good idea or not, just pointing out that some of the early rhetoric was pretty close to what you are describing.
Indeed, when confronted with a potentially massively deadly new and poorly characterized infectious threat it may be reasonable for individual citizens to voluntarily limit social interactions until sufficient information is available, and to avoid overloading the healthcare system. Unfortunately, the Covid lockdowns soon became politicized and being forced from above were not subject to the feedback loops that make voluntary interactions socially efficient. The net effect was trillions of dollars of economic losses, widespread emotional trauma and no lives saved to show for it.
You don't even need to go so far as saying no lives saved. That might be a bit controversial.
You can get a pretty interesting argument by just taking official or mainstream estimates of how many lives were saved and compare them with some reasonable estimates for costs of lockdowns.
If you can get enough data for an estimate, you should use QALYs instead of lives.
(It's a better idea in general, but also allows you to optionally give the lockdowns a cost in terms of quality of life.
Even if life under lockdown only costs something like 1% of quality of life for the duration, it quickly becomes damning, because everyone pays for it.)
> Can we use our improved understanding of disease seasonality against it? (...) At best, it would just put us in the same position as the tropics, where there’s nothing to constrain the disease’s rhythm, and it just strikes randomly.
Arguably, the most important point about corona pandemic is to prevent its spikes. I don't want to downplay the effects of the disease on individuals. (Deaths! Long covid!) But *the* reason for government intervention and lockdowns is the threat that our health systems might get overwhelmed.
For seasonal diseases (and perhaps even now for covid), the tropics are in a much better position because the spikes are smaller. That makes it a lot easier to deal with. It's like for transportation: our roads and public transport must be able to handle rush hours. If we could re-distribute that traffic evenly over the day, we could easily cut down our traffic infrastructure by half.
The total area under the curve is also important. Ie how many QALYs (quality adjusted life years) do we lose in total.
Interventions and treatments should be weighed and compared by how much they cost per QALY rescued.
You can integrate the concern about peaks into the general QALY framework. As you already point out, sizing a system to deal with peaks and troughs either is really expensive or insufficient.
I really wanted to see a comment on cicadas.
How do we know that some diseases that appear seasonal aren't some complex, multi-year dance between communicable pathogens and the collective human immune system (that just happen to coordinate on emergence seasonally, but it's pretty much a distinct cohort each year)?
I definitely don't get the flu every year. More like every 7 years or so. Something something prime numbers....
"Yet I have never heard anyone claim that any winter diseases happen in summer in Arizona or Saudi Arabia or terrible places like that."
That made me curious as to what 'summer diseases' might be circulating in Saudi Arabia (indeed, are there such things as 'summer diseases'?) The closest I came to it was this:
(1) Study titled "Temporal trends in the incidence and demographics of cancers, communicable diseases, and non-communicable diseases in Saudi Arabia over the last decade" https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6468216/ - summation: vaccination programmes are knocking the usual illnesses (measles, smallpox, etc.) on the head, but as Saudi Arabia got richer, the population developed the diseases of affluence (diabetes, obesity, cardiovascular problems).
The incidental line that intrigued me was this -
"Cases of some infectious diseases were recently identified in Saudi Arabia, indicating that despite technological developments in diagnostics, treatment, and vaccination programs, various infectious diseases have re-emerged in Saudi Arabia after a decade. For instance, the prevalence of Middle East respiratory syndrome coronavirus infection increased in Saudi Arabia during 2012, and this disease continues to be a concern during the summer season and religious congregations in holy sites."
Okay! What looks like a summer disease! So that led me on to this:
(2) A study titled "Lack of seasonal variation of Middle East Respiratory Syndrome Coronavirus (MERS-CoV)" https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7128823/
Conclusion: First it *looked* as if there were seasonal peaks, but um, probably not. Also, it has to do with camels.
"Based on the occurrence of initial clusters in April 2012, April–May 2013, and May 2014, it was concluded that there was a significant MERS-CoV activity in March–May of each year. Initial hospital outbreaks also occurred in April 2012 (Zarqa public health hospital, Jordan), April–May 2013 (Al-Hasa Outbreak) and April–May 2014 (Jeddah outbreak). Thus, it was thought that MERS-CoV occurs predominantly during the spring (March–May). The occurrence of cases in the spring raises the possibility of seasonal cycles of MERS-CoV as camels give birth in March (spring) and MERS-CoV occurs commonly in young camels. Seasonal variation may reflect the risk of transmission of MERS-CoV between animals and humans.
...Seasonal variations among the transmission of respiratory viruses reflect the risk of animal-human transmission, difference in the circulating viruses, and the natural reservoirs of specific viruses [4]. Since the emergence of MERS-CoV, it was though that MERS-CoV transmission occurs through two seasons: the spring (March–May) and the fall (September-November). Seasonal variation may occur due to dromedaries’ calving season (November and March). In one study, the prevalence of MERS-CoV was higher among camels in the winter time (71.5%) than the summer time (6.2%).
In an analysis of MERS-CoV cases from June 2012 to July 2016, authors estimated mean monthly data for all the included studies and showed that MERS-CoV may have two peaks in the winter and summer months. However, we showed no definite seasonal variation of primary MERS-CoV cases despite initial peak in February and August 2015 and in March 2017."
So in conclusion - well, I'm not entirely sure what to conclude. A very scanty, cursory look doesn't seem to turn up summer diseases comparable to winter diseases, so the question still remains: why winter peaks?
I'd suggest taking out that 'whatever' about African-Americans getting flu more before someone quotes it out of context as you not caring about the greater rate (obv not what was intended).
Thanks for explaining that. I've been wondering about that forever.
"July in Alaska doesn’t have to outrun January in Florida, it just has to outrun January in Alaska, for the dubious honor of when Alaska’s destined-to-be-once-a-year flu season is going to be."
I think this is backwards (July in Alaska is not Alaska's flu season).
I think it should be "*January in Florida* doesn't have to outrun *July in Alaska*, it just has to outrun *July in Florida* for the dubious honor of when *Florida's* destined-to-be-once-a-year flu season is going to be."
(or alternatively "July in Alaska doesn’t have to outrun January in Florida, it just has to outrun January in Alaska, for the *genuine* honor of when Alaska’s destined-to-be-once-a-year *relatively flu-free* season is going to be", but that's a bit more awkward)
I was imagining "outrunning" as in a contest to not get the flu.
That was what I was getting at with my somewhat awkward "Alternatively..." rephrasing.
Maybe it's just me, but if "outrunning" is in a contest to *not* get the flu, then it's not "for the dubious honor of when Alaska’s destined-to-be-once-a-year flu season is going to be". The metaphor seems to switch direction halfway through the sentence.
Do pathogens really prefer cold temperatures & low humidity? My impression was that the tropics had a higher disease burden than really cold areas.
Keep in mind that different pathogens 'prefer' different things.
Most viruses pretty much have to go from one human directly to another. Lower humidity might allow virus laden droplets to stay in the air for longer, but we are typically talking about minutes here.
In contrast, lice work rather differently. Or worms. Many bacteria have spores. Etc.
Does the natural immunity you get from getting covid last longer than the vaccines? Searching I get different answers.
https://www.nebraskamed.com/COVID/covid-19-studies-natural-immunity-versus-vaccination
https://www.medrxiv.org/content/10.1101/2021.08.24.21262415v1
(This seems like it should be easy to answer by now.)
https://www.science.org/content/article/having-sars-cov-2-once-confers-much-greater-immunity-vaccine-vaccination-remains-vital
OK I've been saying that being vaccinated, I would like to get a small dose of covid. Is there something wrong with this? The whole 'narrative' that everyone must get vaccinated seems to be distorting everything... but I just don't know.
It seems to me that your problem would be getting the dosage right.
The Brits were doing challenge trials of Covid, so those scientists may have figured out how much is "enough."
https://www.bbc.com/news/health-56097088
Yeah, I'm not actively trying to get sick, but covid is rampid (?ravid, sp, all over the place) where I live, (Wyoming county, NY.) Many of the people I'm working with have had it... so I'm just hoping for a little dose. Talking with people at a bar. (I'm working in the kitchen.)
If natural immunity is X times better than vaccine (X>1) then everyone doesn't need a vaccine, only those who haven't had it.
Before we had vaccines, some economists' blogs were speculating about the costs and benefits of giving large swaths of volunteers herd immunity in something like this way.
This is especially tempting, since young healthy people typically get asymptomatic or mild cases, but still suffer from lockdowns just the same.
I will say from experience having lived in both a very cold climate (northern Germany) and a very warm one (Florida), the human body adjusts its setpoints w.r.t. "this is cold" and "this is warm" to its environment: when I moved from Germany to FL, it was January, and I went swimming in the hotel pool because 50°F felt so warm. Is it possible that the thing that matters for disease vulnerability is not absolute temperature, but rather differences in temperature between the warm and cold seasons? Note that I'm not necessarily suggesting that the intensity of the disease cycle is proportional to the magnitude of this difference - simply that there's some threshold temperature difference between seasons above which disease dynamics are governed by that cycle. This would explain why the tropics, which have almost no such difference, have random disease cycles.
I grew up in Germany, but now live in Singapore.
The weather here has very mild seasonality in terms of temperature only. But we do get a fair bit of seasonal variation in rainfall.
What's really striking me is the near constant day length.
Even though some people have made related points, it gives a lot of insight to make a (simple) calculation with numbers in a very simple infection model.
The reproduction value R is the product of two factors:
- An intrinsic value R_0: how many people an average person infects in a population without immunity.
- A dynamic factor x: what percentage of people are currently susceptible (not immune).
Then R = R_0 *x. We all know now that an epidemic spreads when R>1, and does not spread if R<1.
Without seasons, R_0 remains constant, and R stays at equilibrium, R=1. On each day a few people lose their immunity. Let's say that immunity lasts for 200 days, then roughly 1/200 = 0.5% of the population become newly susceptible each day. This means that x increases by 0.5 percent points, and so R increases as well:
R = R_0 * (x_old + 0.5%) > 1 .
So the infection spreads, but not for long. As soon as 0.5 percent of the population have caught the disease, x goes down to its original value. Then R=1, and the system is back to equilibrium. This basically happens every day.
But what happens if we have seasons? This is a relatively sudden event that increases R_0. Let's say R_0 suddenly goes up by 10%, so by a factor of 1.1. Then R becomes
R = R_0_old*1.1 * x > 1.
So the infection spreads, and it spreads until x has decreased by a factor of 1.1. That is the case when roughly 10% of the susceptible people have been infected. So there is potential for a sudden surge of diseases, so a wave.
The point is that this is pretty independent of whether you live in Alaska or Arizona, even if they have very different base values of R_0. If R_0 suddenly increases by 10%, then ~10% of susceptible people will catch it before equilibrium is reached again. The main difference is that if Alaska has a higher base value of R_0, then fewer people will be susceptible in equilibrium, so we would expect a slightly *less* strong wave. But not by much. Let's say Alaska has 20% higher base value of R_0 than Arizona, then it will have ~20% fewer susceptible people, and the Alaska wave will be lower by 20%. My point is that this is not much of a difference, even though the difference between Alaska and Arizona is huge in this scenario: it would mean that even the winter in Arizona would *still* be 10% better than the summer in Alaska.
It bothers me a bit that the size of the wave in this model is "only" 20-fold larger than in the model without seasons, but I am not at all sure about the numbers. In 200 days after infection, you have lost some of your immunity, but you are not back to baseline. For seasonality, it's estimated that corona has 20-30% higher R-value in winter. (Studies which only take data from Europe even get 40% or more, but the data is probably pretty confounded.) I am not sure how sudden this change is. Does a lot of this happen in just a week or two?
Another thing is that this is a very simplistic model. For example, populations are not homogeneous, mixing is a non-trivial thing, and there are non-negligible delays. I would guess that real-world waves tend to overshoot the theoretical equilibrium for various reasons.
If you haven't seen it, you might want to take a look at this article:
<i>Abstract
Viral respiratory diseases (VRDs), such as influenza and COVID-19, are thought to spread faster during winter than during summer. It has been previously argued that cold and dry conditions are more conducive to the transmission of VRDs than warm and humid climates, although this relationship appears restricted to temperate regions and the causal relationship is not well understood. The severe acute respiratory syndrome coronavirus 2 causing COVID-19 has emerged as a serious global public health problem after the first COVID-19 reports in Wuhan, China, in late 2019. It is still unclear whether this novel respiratory disease will ultimately prove to be a seasonal endemic disease. Here, we suggest that air drying capacity (ADC; an atmospheric state variable that controls the fate/evolution of the virus-laden droplets) and ultraviolet radiation (UV) are probable environmental determinants in shaping the transmission of COVID-19 at the seasonal time scale. These variables, unlike temperature and humidity, provide a physically based framework consistent with the apparent seasonal variability in COVID-19 and prevalent across a broad range of climates (e.g., Germany and India). Since this disease is known to be influenced by the compounding effect of social, biological, and environmental determinants, this study does not claim that these environmental determinants exclusively shape the seasonality of COVID-19. However, we argue that ADC and UV play a significant role in COVID-19 dynamics at the seasonal scale. These findings could help guide the development of a sound adaptation strategy against the pandemic over the coming seasons.</i>
https://agupubs.onlinelibrary.wiley.com/doi/10.1029/2021GH000413
One thing that is important to note is that you shouldn't trust CDC or WHO flu data. The CDC deliberately inflates flu data to encourage people to get the flu shot. They do this by including pneumonia deaths in flu deaths when they occur during "flu season". So, a lot of the seasonality of flu deaths comes from the CDC's method of counting them.
I know this sounds like a wild conspiracy theory, but this point was brought up in an opinion piece by a Harvard Medical School professor in Scientific American (https://blogs.scientificamerican.com/observations/comparing-covid-19-deaths-to-flu-deaths-is-like-comparing-apples-to-oranges/) and it's pretty easy to check if you go into the details of the actual report.
*I put this comment on the r/ssc subreddit as well, but I thought I'd crosspost here so more people could see it.
This is pretty shocking. I found another complaint against this policy, some sort of internal memo [1]. The author cites the NCHS death statistics from 2001 [2], pointing out that of 62,034 deaths from "pneumonia and influenza", "61,777 ... were attributed to pneumonia and 257 to flu". It seems unlikely that the flu led to pneumonia 100% of the time. The CDC explains that the reason deaths are lumped together is to correct the underreporting of flu on death certificates [3], but this seems like a massive overcorrection. I can't really see why the CDC would make such an obvious error if not to encourage people to get their flu shot, wash their hands, etc. as the article you cite suggests. This seems (as far as I can tell) to be a blatant misrepresentation of the facts, which is quite upsetting.
[1] https://aspe.hhs.gov/cdc-influenza-deaths-request-correction-rfc#main-content
[2] https://www.cdc.gov/nchs/data/nvsr/nvsr52/nvsr52_03.pdf
[3] https://www.cdc.gov/flu/about/burden/how-cdc-estimates.htm
Hmm, I'm just wondering how many covid deaths are from people who get covid and then pneumonia? And yeah I have zero trust in what my government tells me... sad.
This is a good source for looking at how Covid deaths are recorded: https://www.cdc.gov/nchs/data/nvss/vsrg/vsrg03-508.pdf
Also this article was pretty helpful for helping me understand how it all works: https://www.aamc.org/news-insights/how-are-covid-19-deaths-counted-it-s-complicated
I would guess there are far fewer edge cases now that testing is easier and widely available. Based on the CDC document I linked above, it looks like it's up to individual doctors to decide how to report deaths associated with Covid. In order to make the case that there's serious over-reporting of Covid deaths going on, you'd have to find a compelling reason doctors/nurses would choose to over-report. Maybe more funding? Better health insurance payouts? I don't know, but I doubt it's a big problem anymore.
Okay, the data from 2015 paints a much less extreme picture. 5,251 influenza deaths and 51,811 pneumonia deaths [1]. This would suggest a big change in behavior in doctors/nurses filling out death certificates; they have become much more likely to report influenza as the underlying cause of death for a patient. The underreporting the CDC is complaining about seems to have gotten less severe. From what I’ve read about death certificates though, it seems like the flu could have a lot more deaths attributed to it than what would seem plausible. Perhaps the CDC is being dishonest, but I doubt they would have done so if they had more reliable statistics to report.
It also suggests that the professor you’re citing is being misleading. From what I’ve read about Covid, I would guess many older people, especially those with pre-existing respiratory conditions are quite vulnerable to the flu. Whether they die from the influenza virus (viraemia) or some other reaction to it (cardiac arrest, ARDS, etc.) is irrelevant. So his report that he has had no patients who died directly from the flu is not very meaningful.
It’s still crazy to me that so much of the scientific and policymaking world has no idea about the discrepancies in these statistics. It suggests that the CDC needs to rearrange its priorities in favor of telling the public the truth rather than what’s “good” for them.
[1] https://www.cdc.gov/nchs/data/dvs/LCWK10_2015.pdf
The fact of the matter is that very few people ever receive laboratory tests for influenza relative to the number of people who report with symptoms consistent with influenza infection, which is why you often see reference to the term "influenza-like illness" during the flu season. The only way to try to recover the number of influenza-related deaths (which should include secondary pneumonias and other downstream complications, as you suggest) is to do so indirectly by combining what's known about the case mix and outcomes among those with confirmed influenza with outside information (e.g., death certificates, hospitalization rates). All that modeling obviously involves assumptions and the attendant uncertainty.
If you read the second paper cited on the CDC's page explaining how they calculate influenza burden (Rolfes et al.), you'll see they do report ranges that suggest considerable uncertainty in burden and death estimates. Speaking as someone who's worked a little on flu and other infectious diseases subject to similar limitations in data capture, I think it is less accurate to report deaths with lab-confirmed influenza as the only deaths due to influenza. You have to do modeling or statistical correction to at least partially account for the considerable shortcomings of surveillance data.
I am a cat and not an epidemiologist, but when polio outbreaks were still a thing, didn't they mostly occur in the summer?
Yes, in temperate zones polio was seasonal with peak in summer/autumn. But it's not a respiratory virus, and it spreads via the fecal-oral route. I'd guess that swimming was the seasonality factor for polio.
Do we really trust the panda more than the cat?
Trust the panda. I do recall stories of pool closings during polio outbreaks.
Panda and cat didn't disagree anyway?
Children are disease vectors. They haven't yet built up immunity to as many diseases as adults and they have terrible hygiene. I wonder if kids going back to school in the fall kick-starts the disease season, and it peaks a few months later after spreading through the community?
Obvious way to disprove this: look at countries that don't take summer vacations, or that take their extended school vacations during some other season.
Section III sounds like a coupled harmonic system that naturally synchronizes. I remember studying this in intermediate dynamics class.
Here is the classic metronome synchronization experiment that demonstrates it:
https://www.youtube.com/watch?v=T58lGKREubo
Here is Veritasium's non-mathematical explanation:
https://www.youtube.com/watch?v=t-_VPRCtiUg
Note that epidemological models are nonlinear so they can produce much more complex behaviours than a harmonic oscillator can when driven in this way. There's all sorts of bifurcations and chaos theory going on.
I was just reading about a (testable) hypothesis called Temperature Dependent Viral Tropism in a paper by Shaw Stewart and Bach. Here's a link (but, you know, search if this link gets nerfed).
https://www.researchgate.net/publication/351308807_Temperature_dependent_viral_tropism_understanding_viral_seasonality_and_pathogenicity_as_applied_to_the_avoidance_and_treatment_of_endemic_viral_respiratory_illnesses
I'm not endorsing this or saying this is True but it seems on topic and interesting.
I find some of the ideas in this article fascinating, specifically:
* Spraying of class 2 biosolids + seasonal wind currents driving pandemic waves
* Seasonality has partially hid that COVID-19 is really probably COVID-18
https://theethicalskeptic.com/2021/11/15/chinas-ccp-concealed-sars-cov-2-presence-in-china-as-far-back-as-march-2018/
Re: both cold winters and hot summers forcing people inside: perhaps so, but I cuddle with the people in my house a lot less during hot summers than cold winters.
I think 'forcing people inside' is just a simplified reference to all behavioral adaptations to cold seasons, which are manifold. Maybe winter coats that gets used constantly and never get washed are transmission vectors, maybe indoor heating is a better vector than indoor AC, maybe people indeed cuddle more when it's cold.
Not that I think this overturns the rest of the analysis or anything, but I think it's relevant as a 'reality has a surprising amount of detail' thing. You can't just dismiss the whole topic of cold weather behavioral adaptations because someone summarized it as 'people staying inside more' and that summary is disproveable.
__init__Oct 23 (https://astralcodexten.substack.com/p/chilling-effects)
If HxNy were the only flu strain, we would approach herd immunity within several years, even through a cold winter. So the flu continues to mutate into different strains to evade immunity, and one of the major unmentioned factors here is this strain churn, means a (in reality, a set of dozens of) different strains circulates through populations each year. The consistent cyclicality of flu season is largely driven by strain churn, but that still doesn't explain the peak/trough and their correlation to seasons.
I'd speculate summer as the selection bottleneck in highly seasonal regions, and winter as the exponential part of infection S-curve. So: it's summer is northern Eurasia, and the living is easy, except for the immuno-compromised. Which strain is best able to make it through the summer? This is largely driven by which strain does the immune system have the least memory of. And since the immuno-compromised are usually old, this is perfect for finding something most other people have never been exposed to either.
Now it's September, and the flu has just faced a 99% mass extinction event - especially around the previous year's strain where R0 is approaching less than one. Whichever funky new (so old, it's new) strain was able to hang on and continue to infect is going to well poised to spread through the rest of the population. Through travel, hajj's, agrarian laborers etc, these selected for strains again move throughout the world causing another peak. Immunity to the new strain builds, and then we do the summer selection process all over again.
> Yet I have never heard anyone claim that any winter diseases happen in summer in Arizona or Saudi Arabia or terrible places like that.
No? I lived in a place like Arizona or Saudi Arabia, and if I remember correctly the consensus was that people always seemed to get sick when the weather changed; either from hot->cold or cold->hot.
Why is it so implausible that human beings themselves exhibit seasonality that nobody ever mentions it as a possibility? For most of human history, the differences in energy availability between summer and winter have been pretty large. Is it really that unlikely that we have vestigial evolutionary adaptations to reduce energy consumption during winter that could affect our immune systems?
Like: could it be that there is an evolutionary advantage to killing off the old and frail during the winter months when they would otherwise be diverting scarce nutritional resources from the young and healthy. Disease seasonality is a feature, not a bug.
That mechanisms would have to directly benefit the genes of those old and frail. Evolution (by and large) doesn't run on group selection.
See eg https://www.lesswrong.com/posts/QsMJQSFj7WfoTMNgW/the-tragedy-of-group-selectionism
I think one way to think about it is to consider the fact that the smallish seasonal advantages/disadvantages affect the reproduction number, which affects the number of cases logistically (in simple models). If R_0 is 0.9 for some virus in the summer and 1.1 in the winter, this does not mean that about 20% more people will be infected in the winter as compared to the summer.
Instead, it means that the virus will be dying out in the summer and grow exponentially at the beginning of winter.
For covid-19, it feels like R_0 is varying a lot more than 0.2 between the seasons. I mean, people are generally not stupid {{Citation needed}}. They might not be 100x as careful if the incidence is 100x as high as during summer, but they still will probably take additional measures sufficient to affect R to a measurable degree.
I am a bit confused about this temporary immunity thing. Evolutionary, memory cells make a lot of sense, which is why we have them, I guess. Is it just that having antibodies around allows for a quicker response, and that these tend to decrease over a few months?
Virus mutations will complicate matters, of course. Naively, I would expect the possibilities for mutation of a virus to be proportional to the number of infections. While recent viruses might travel between hemispheres twice a year, earlier ones were probably more at home in a single hemisphere? This would mean that the maximum proliferation of new variants coincides with maximum incidence. So to explain multiple waves, one would either have to assume mostly separate populations between which the virus can only travel occasionally or to assume temporary herd immunity again: 'Most mutations are created when infection rates are highest, but they initially can not spread far because of herd immunity. Only after herd immunity is decreased after a few months (or a year) can the mutations prove their merit by out-competing the other variants.'
Or it might be that hosts with a somewhat compromised immune system are not only the perfect places to stay during times of R<0, but also to acquire new mutations to evade existing immune responses.
I thiiink RJ, Brazil, is having a big flu outbreak now (I imagine it normally happens in winter? should check). Maybe the lack of a strong flu season in winter due to covid precautions screwed up the zeitegstgneber
my intuition is that you get seasonality under very broad assumptions (r0>1 and varies seasonally, immunity wanes on the order of at least a year) and the difference is made up by more people needing to get ill to get to herd immunity.
rt should be 1 on average in the long run
I think if we're comparing Alaska in the summer (rt<1) vs Florida in the winter (rt>1) the exponential growth/decay in cases should probably swamp the larger number of cases you'd get in Florida averaged over a year
someone should actually run the number here though
*ed: you'd get in Alaska
https://twitter.com/pawnofcthulhu/status/1468801244793765892
OK I'm not the first person to think of this but here are some simulations
The tropics seem like they undermine this idea, but I want to get it out there:
Seasonality doesn't need to be caused by any external influence.
Consider cicadas. They have a normal seasonal profile of showing up during the weather they like, summer.
But there are also the 13-year and 17-year cicadas. They have a "seasonal" profile of spiking every 13 or 17 years. Nobody believes there's anything special about those years other than the surprisingly large number of cicadas coming out of the ground. Rather than an influence of the environment on the periodical cicadas, this is a special behavior of the cicadas.
There's no reason to believe a disease couldn't accomplish the same thing. Maybe diseases are seasonal because it's part of their life strategy.
That life strategy doesn't happen in a vacuum. So just calling it a life strategy doesn't anwer the question, it just gives the eventual answer a name.
From what I've heard, cicadas have to deal with predators, and that drives their prime numbered cycles.
For diseases, they have to deal with all the factors mentioned in the article.
> From what I've heard, cicadas have to deal with predators, and that drives their prime numbered cycles.
This isn't a real objection. Everything has to deal with predators. The predators have zero explanatory power for why the cycles happen in some cicadas.
They also have zero explanatory power for *how* the cycles happen in cicadas. And while you seem to want to talk about why the cycles happen, the topic of the post is how.
> So just calling it a life strategy doesn't anwer the question, it just gives the eventual answer a name.
Calling periodic behavior a life strategy answers the question of why it's happening. ("Because the organism is designed to do things that way.") This is conceptually separate from why doing things that way might be advantageous to the organism (Maybe it isn't! Warblers feed cuckoos because their design includes behavior that causes them to do that, despite the fact that feeding cuckoos is hugely disadvantageous.), and from how the behavior occurs.
I'm here to point out that the post above us is implicitly but very strongly committed to the idea that the cause of disease seasonality is to be found in environmental conditions, and this assumption is not actually warranted. Seasonality could be a behavior that the disease coordinates itself. In other words, the post is committed to an idea of *how* seasonality occurs that I believe bears further critical examination. The cicadas are an example of seasonality occuring without any reference to local environmental conditions. If cicadas can do it, diseases can do it to.
Why not have the greater infections during the winter be not a result of anything to do with the virus itself, but be determined by an intrinsic seasonal adjustment of the human immune system? That way it would be independent of the place because the people living in that place would come to recognize "winter" and "summer" and configure their immune systems accordingly.
Testable prediction of this theory: This means that someone who moved from one place to another might trick their immune system into being confused about what season it is and they would then be "out of sync" and thus more/less susceptible to viruses than the rest of the people living in the area who have been living there for a long time.
Your prediction can be broadened to include travelers. Especially when you compare travelers within hemisphere to those crossing the equator. (So that you can largely eliminate the influence of travel by itself as a factor.)
Slight complication: it's hard to observe the state of the immune system directly. And observing whether someone catches a cold or not, depends on whether a cold is going around just as much as the stand of their immune system.
1. Flu vaccines don't work well enough to explain the difference in influenza rates that black people experience.
2. COVID vaccines reduce hospitalizations and deaths but do not reduce case rates in any substantial way.
3. Neither of the above should be confused with other vaccines like, for example, MMR (measles mumps rubella) which are extremely effective and provide sterilizing immunity for years.
This is a very interesting take on COVID, influenza, and seasonality:
https://eugyppius.substack.com/p/the-disappearance-of-influenza
Do the flue vaccines not work so well, because there are so many strains (and the guess about what to vaccinate against is typically slightly wrong)? Or is the reason that they don't work so well in general, even when the guess is perfect?
PS The BCG vaccine is very interesting. Depending on country, it sometimes seems to provide no protection at all against the disease it's meant for, but it still lowers total mortality.
In South East Asia, we have two flu seasons a year - a summer season and a winter season - for EXACTLY the reason you mention - in the summer, people coop themselves up at home with the air-conditioning on full blast.
In the west, shade is adequate to cool you in the summer, so you don't need to close the windows and turn on the A/C. In South East Asia, the muggy air retains heat, requiring air-conditioning and reduced airflow.
I'm not sure what you mean by 'the west'. Florida is certainly west of South East Asia, but I don't think shade will make it bearable enough?
I'm living in Singapore at the moment, and we still get two flu seasons, despite there being no winter nor summer to speak of.
Why doesn't that affect the United States east coast? The Bay Area has dry heat, as does the rest of the North American Pacific coast (though I'm not sure about Baja California, being a penisula), but even the cold parts of the eastern US have very muggy summers. Closing all the windows and shades is sometimes sufficient in the colder parts, but anywhere from Maryland south it is not, A/C is mandatory. This also applies to most of the Gulf Coast states - everywhere east of Texas, and some parts of Texas.
The vast majority of the population in SE Asia doesn't have in-home air conditioning. They have windows and fans. While they would *like* to close themselves up in an air conditioned sealed house, we just don't live in a reality where that is possible for anyone but the wealthy.
There are some countries where AC is more common like Singapore and Taiwan, but their populations are absolutely tiny compared to the populations of Philippines and Thailand.
Same thing seems to happen in Houston, TX with COVID-19. One peak in the summer and another in the winter.
https://www.tmc.edu/coronavirus-updates/total-tmc-covid-19-positive-patients-in-hospital/
Presumably within a given geographic area, our own immune systems collectively amplify seasonality, since immunity wanes over time.
Have you considered the match between covid-19 seasonality in the US and Hope-Simpson's chart from the Spanish flu? https://twitter.com/Hold2LLC/status/1286549487687696385
Scott, have you seen the Temperature-Dependent Viral Tropism hypothesis, or TDVT?
The basic claim is that viruses evolve to thrive at temperatures below body temperature, to avoid infecting vital organs, to maximize host longevity and mobility, to maximize transmission and reproduction.
It sounds as plausible as some of the other metrics in this post. Here's a preprint: https://www.preprints.org/manuscript/202103.0034/v1