On the Epidemiology of Influenza (2008)
virologyj.biomedcentral.com
virologyj.biomedcentral.com
For example, if you're trying to measure the R number, then you're sampling from a very fat tailed distribution, so it's easy to underestimate.
It also means that if an intervention (such as vitamin D) prevents transmission but not illness, it could be hard to detect/measure the impact.
(This comment is not a summary of the paper)
[0]: https://web.archive.org/web/20130508081643/http://www.scienc...
In 2019-2020 Alberta had 1,595 hospitalized and 41 deaths. This year Alberta had 0 cases of lab tested influenza. That's how much of an effect the current COVID restrictions and renewed awareness of the flu vaccine had on the virus. I'm sure just wearing a mask when you're obviously sick would help close that gap.
So I would be very surprised (and see no indication) that doctors suddenly stopped doing standard diagnostics.
https://globalnews.ca/news/7606557/alberta-2020-2021-flu-sea...
I think wearing a mask when you feel sick and possibly masking up en masse for certain seasons of the year, if it has a measurable impact, is worth it. I really don't mid wearing my mask so if Nov., Dec., and Jan. I have to wear a mask in stores I really don't care at all.
I'm cautiously optimistic that it can take hold in the West this time around.
This analysis reads to me as so out-of-touch as to be other-worldly. Have we already forgotten that there was an incredibly widespread respiratory pathogen through virtually every corner of the world last year?
How can you point to horizontal interdiction as a likely (hell, plausible) explanation when the most obvious is a simple incident of viral interference?
How does the horizontal interdiction theory explain that influenza was similarly suppressed even in places that had no such measures?
What about the apparent suppression of the other four endemic coronaviruses? And the rhinoviruses? How did every respiratory pathogen except one succumb to interdiction (even in places where there was no interdiction), while that one other flourished?
Assume you have two pathogens A and B that are transmissible. A with a reproductive number of 3 and B with an R of 1.5. Now the pool of susceptibles behaves in such a way that only, say, half of transmissions occur. Then pathogen A will die out while B grows exponentially.
> What about the apparent suppression of the other four endemic coronaviruses? And the rhinoviruses? How did every respiratory pathogen except one succumb to interdiction (even in places where there was no interdiction), while that one other flourished?
From speaking to an ENT doctor there were indeed very little respiratory infections (apart from Covid of course).
> How did every respiratory pathogen except one succumb to interdiction (even in places where there was no interdiction)
Not sure what you mean by interdiction - lockdowns are only a proxy for human behaviour. If you have data that indeed influenza was suppressed with no behaviour change and/or seasonality that would be appreciated.
Indeed this is a good scenario for consideration.
Next, to advance the theory in places where horizontal measures were taken, we'd need evidence that R of SARS-CoV-2 is sufficiently higher than other respiratory pathogens. Even if this is true for influenza (and sure, it might be), it seems unlikely to be true for the other four endemic coronaviruses.
> From speaking to an ENT doctor there were indeed very little respiratory infections (apart from Covid of course).
Right. And you don't need the anecdote; we know this from ILInet.
> Not sure what you mean by interdiction - lockdowns are only a proxy for human behaviour. If you have data that indeed influenza was suppressed with no behaviour change and/or seasonality that would be appreciated.
How do you explain the similar suppression in Sweden, Florida, Haiti, etc.? Places that had:
1) No serious interdiction to speak of, and 2) Fairly rapid achievement of endemic equilibrium in SARS-CoV-2
...also experienced suppression not only of influenza but of the other four endemic coronaviruses and both rhinoviruses.
The unambiguous Occam's Razor - and the explanation most established by historical study on these matters - is that we're seeing a case of viral interference.
I already stated the explanation: lockdowns/measures are only a proxy for human behaviour. Measures don't stop the spread per se, humans do.
E.g. in the case of Sweden (can't speak for the other examples) human behaviour drastically changed (e.g. see mobility data). Yes, Sweden did not implement curfews and generally did not close schools but still had quarantine rules, social distancing, masks, travel restrictions and strong guidance of personal responsibility, not to come to work when sick, hygiene etc.
I would be very surprised if this did not result in a suppression of other pathogens, too.
> 2) Fairly rapid achievement of endemic equilibrium in SARS-CoV-2
Unfortunately the situation in Sweden is what it is: Hit hard by a second and now third wave, and significantly more cases/deaths than neighbouring countries (not saying there are no benefits, it's just a different trade-off).
By the way if you look at case counts from other European countries during the first wave you will see the same pattern: Case counts start to decline before lockdowns become effective.
> we're seeing a case of viral interference.
If there is evidence or even just anecdata I'm intrigued - I don't see it yet.
>> we're seeing a case of viral interference.
> If there is evidence or even just anecdata I'm intrigued - I don't see it yet.
Norovirus had a really bad year in 2020. From the standpoint of the virus. Norovirus spreads by fomites not respiratory droplets. Basically completely orthogonal virus to covid.
Now, I admit, I haven't been to Sweden to observe the human behaviors you're discussing, but I am in Florida, and I can tell you without any doubt that, while there have been substantial vertical stratification measures (young people staying away from old people), there have been virtually zero horizontal measures. People gather in numbers every evening without masks. Schools have been open the entire time. There is no meaningful social distancing within risk tiers.
So I'm interested to hear an explanation of how this selective suppression can possibly be explained by human behavior in this case.
I think we need to pause to note: viral interference is a well-documented phenomenon, and everything about this situation is consistent with what we know of it. Selective suppression of a class of aerosol-mediated respiratory pathogens, on the other hand, is unknown to medical history.
So which is more likely?
> If there is evidence or even just anecdata I'm intrigued - I don't see it yet.
I don't understand this part - the evidence is identical. The question is, which phenomenon does the evidence indicate?
And the answer is clear: there's nothing at all that suggests this is based on human behavior (even if that were a documented phenomenon, which it isn't), while it fits with great precision the characteristics of viral interference (a widely studied and well-documented phenomenon).
Not only does it generally fit the pattern of viral interference, but it even specifically fits the pattern of viral interference in influenza[0].
So, let me ask you the same question: what evidence do you have to refute the conclusion that this is part of a documented phenomenon, and instead support the conclusion that it's part of an unprecedented and seemingly self-contradictory phenomenon?
These sort of measures and proposals read as if you are talking about livestock, not humans.
youtube.com/watch?v=D3IteYQ7xhc
It's crazy how little attention this is getting. We're living through a global pandemic of a respiratory virus that predominantly affects the elderly (with weakened immune systems) and the immune-compromised, and almost no one is interested in this.