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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.

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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?

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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.

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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.

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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?

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Could pathogens be affected by the moon? Maybe seasonal disease come and go like the tide?

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“ 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.

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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?

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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.

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Perhaps with all the vegetation going dormant in the winter there is just poorer air quality?

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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.

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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.

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Maybe more people swimming in salt water during the summer months kills off a lot of pathogens?

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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).

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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...

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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.

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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.

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> 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?

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"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.

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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."

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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.

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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.

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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."

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> 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.

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"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.

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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).

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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.

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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

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> 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.

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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.

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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.

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> 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.

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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....

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"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?

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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).

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Thanks for explaining that. I've been wondering about that forever.

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"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)

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Do pathogens really prefer cold temperatures & low humidity? My impression was that the tropics had a higher disease burden than really cold areas.

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Does the natural immunity you get from getting covid last longer than the vaccines? Searching I get different answers.



(This seems like it should be easy to answer by now.)

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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.

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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.

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If you haven't seen it, you might want to take a look at this article:


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>


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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.

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I am a cat and not an epidemiologist, but when polio outbreaks were still a thing, didn't they mostly occur in the summer?

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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.

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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:


Here is Veritasium's non-mathematical explanation:


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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).


I'm not endorsing this or saying this is True but it seems on topic and interesting.

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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


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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.

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__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.

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> 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.

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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?

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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.

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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

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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

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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.

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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.

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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:


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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.

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Presumably within a given geographic area, our own immune systems collectively amplify seasonality, since immunity wanes over time.

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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

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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

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