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Do we really know why seasonal respiratory viruses are seasonal?


Apiery

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Vitamin D's primary role is to allow gene expression to vary with the season.
Do seasonal respiratory viruses make use of this seasonal variation in host tactics?
Let's call this hypothesis H.
We don't need evolutionary game theory to consider H plausible, but such a model will be sketched below.
We know that virus droplet vectors lose effectiveness in warm and wet conditions.
It is widely believed that this physical limitation is what accounts for their seasonality.
Let's call this hypothesis W.
 
W is in considerable tension with our modern climate-controlled overwhelmingly indoor lifestyles.
Why should it depend so strongly on the weather when we are almost all most always indoors?
Perhaps then their seasonality really could primarily be caused by the vitamin D status in the host?
There are certainly plenty of physiological changes induced by it to potentially entrain to.
Let's call this hypothesis D. D is just one pathway in which H might occur. Multiple pathways can occur at once.
 
We should be interested in whether H by means of D is a better explanation than W.
 
The COVID-19 pandemic is a tragic crisis but the wealth of information it provides gives hope.
Close examination of the resulting global scale natural 'laboratory' suggests that COVID-19's spread does not depend on weather.
Again another tension with W.
Is there a convincing W compatible alternative explanation given out there?
If not why shouldn't we just suppose D is likely?
 
The biologically active form of vitamin D is calcitriol.
It fits like a key into the vitamin D receptor which then tweaks the mix of proteins that are made by the cell.
Many changes then happen but the innate immunity is the immediately salient choice for primary channel through which information would flow from host to virus.
 
A test screening for chemicals active against COVID-19 found that calcitriol was active.
This is interesting because it is a fairly inert chemical.
Does it directly chemically assault the virus? Perhaps by undermining the integrity of the envelope?
That's what I had been unthinkingly assuming until thinking about hypothesis D made me realize that another possibility was on the table.
Unfortunately I don't have the required background knowledge to even understand what the experimental setup is here.
Would someone kindly explain it to me? I would be most appreciative.
I am thinking that perhaps it is actually direct laboratory evidence that calcitriol induces changes which effectively signal 'slow down' to the virus.
 
Ok, what's with all of this anthropomorphic talk about signals and such?
Well might intuitively think of us hosts as somehow in competition with the virus.
But the hosts are really the environment for the virus.
Does it even make sense for an environment to be in competition with its organisms?
The proper analogy is not one of competition among peers but one of communication between entities which are mathematically *dual*.
A host environment is dual to a herd of viruses.
 
By dual here I simply mean that we can swap the roles we choose to see them as. Whatever is filling the role of an environment factor becomes a herd instead and vice versa.
But of course we already know this because we normally think of hosts as organisms and organisms come in herds.
And it's quite normal to think of a virus as a factor in the fitness environment for a herd of organisms.
 
Herds and their environments must communicate and they do so by changing the fitness landscape of one another. This actually works whether or not the environment is itself entirely biological. Thus ecology arises. Ecology is the fully self-dual perspective on evolving systems.
This is all part of the evolutionary game theoretic perspective on viruses. The math is quite beautiful.
 
The real world point is just that we a priori expect to see how the host environment communicates to the virus by seeing how it culls the virus herd either directly or indirectly.
The direct channel is the one with the highest bandwidth. I contend that for the above basic (yet deep) reasons that, in this case, it is the change in seasonal fitness landscape of the vitamin D innate immunity vs. adaptive immunity which most efficiently conveys what season it is outside to a virus restricted to looking for cues from the inside. I mean what's your thermostat set to? Seems a might strange that the virus doesn't seem to behave the same all year around when the thermostat hardly moves throughout the year.
If the innate immunity keeps numbers in check then the adaptive immunity will accumulate information about the adversary more slowly. This lets the virus conserve hosts in its lean summer times when its droplets spread poorly. In the winter it can spread efficiently to new herds by inducing the host to cough by provoking the adaptive immune system. The fundamental physical temperature and humidity limitation of droplets is what ultimately gives the virus a season dependent preference in tactics.
This all works smoothly when infecting a usual host. When crossing between species the tuned balance of the host/virus ecosystem is thrown out the window.
 
The upshot of all of this is that if you can get enough activated vitamin D (Calcitriol) flowing around in a patient early enough then you plausibly would be able to treat COVID-19.
There was one such RCT from some months ago which reported exactly this. It has been underappreciated in large part thanks to statistical blinding failings and the usually understandable norm of refusing to take small studies with irregularities and results which are "too good to be true" seriously.
I have done my best to analyze it as objectively as a mathematician without prior statistical experience can. By thinking carefully through it at the probability level, one is virtually forced to accept that the study is either true or someone committed fraud. I asked r/statistics if they could find a way in which the ridiculously positive results could be explained without fraud or gross incompetence. I did not get a straight answer.
If you will let me speak of game theoretic signals one last time... This is ought to be the maximum signal that a study can send. In a more virtuous world, the researchers would be seen to have bet their careers on the result. Instead we live in a world where epistemic game theory is not yet a practical thing, I guess. It's not hard to get a feel for how it works though. It's really just a form of liar's dice for scientists. A team of scientists describe how to replicate a collection of dice and then they claim to have rolled them a certain way and got a certain set of results. Ultimately its all just paper though. Why believe some scribbles on a pdf? In order for it to not just be a bunch of meaningless cheap talk there must be something wagered. Reputation is what is wagered and the lower the p-value the larger the wager. We really ought to take sharp notice of such astronomically low p-values even if only for the virtue of identifying fraudsters.
In light of the above and many other corroborating lines of evidence from distinct avenues I think that hypothesis D is strongly warranted for considerable discussion. It seems to be the most efficient explanation of the observed facts. Furthermore the standard of evidence necessary is proportional to the potential health risk incurred. Very low risk together with even just a moderate probability of benefit implies a lower standard of evidence.
I've been at this for a bit and so have others. I am personally at the point where I have almost lost hope that anyone will listen. If you think this warrants professional discussion please bring it up with a peer or maybe a superior. I'm not sure what else I can do or even where to post this. But this is the best explication I can give.
Thank you for your time.
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First of all I will say that COVID-19 should not be lumped together with other known seasonal diseases. The reason is that for the latter the susceptibility is massively lower than for a novel disease. Ultimately, COVID-19 might eventually become seasonal, depending how immunity against it pans out in the population.

The next question would then to look at known diseases and inspect their pattern of seasonality before we go any deeper in specifics. A lot of diseases not only have different patterns, but also different causes, for examples the properties of the causative agent (e.g. mutation rate, sensitivity to temp or humidity etc.), the way it is transmitted (e.g. seasonality of vectors such as tics) and/or human behaviour (e.g. travel pattern). 

Measles transmission cycles have been connected to congregation of children during school terms (see Fine and Clarkson, Int. J. Epidemiol. 1982;11:5-14). If we go for influenza, for example, Vitamin D is one of the factors that have been discussed in terms of seasonality (which falls under host health status) that is potentially one element. But while the seasonality in tropical and subtropical areas does not follow seasons, it still has (short) cycles, which could for example be related to immune responses (e.g. new mutations, followed by infection/vaccination cycles). But indoor heating and ambient temperature have also been linked to contribute to seasonality (or cycles in outbreaks in general).

There are quite a few papers and reviews out there looking especially at these issues. But again, COVID-19 (or spread of SARS-CoV-2) is a special case and would need more time to figure out whether there is seasonality or not.

But perhaps a concise answer to OP, we know to some degree, certainly not for all diseases, and chances are is no universal pattern.

 

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