On the Epidemiology of Influenza (2008)(virologyj.biomedcentral.com)
virologyj.biomedcentral.com
On the Epidemiology of Influenza (2008)
https://virologyj.biomedcentral.com/articles/10.1186/1743-422X-5-29
34 comments
Current flu vaccines don't work very well in old people, due to their weakening immune systems. There is now a high dose inactivated flu vaccine available in the US that also contains adjuvent to partially address this issue[0], but an mRNA flu vaccine would probably help even more. In theory, I think it would be preferable if each person over 55 would receive one dose of the current high dose vaccine in October of each year and be given a silicone P100 respirator, and then be given a booster in December.
[0]: https://web.archive.org/web/20130508081643/http://www.scienc...
[0]: https://web.archive.org/web/20130508081643/http://www.scienc...
So your plan is that everyone over 55 be forced to wear a super serious level of mask for... is it at least three months of the year, or do you just mean "for the rest of their lives"?
No, just provide it to them. I don't expect lots of them to wear it, but I think it would be better to do so than not.
Or we could just normalize wearing a mask when you're sick along with good hand and face hygiene. The outstanding success of the last flu season let's us know that if we take it seriously it should be relatively easy to markedly reduce the misery caused by the flu to a fraction of what it was before COVID.
A fringe of the scientific advisors to various Western governments for the COVID epidemic have given interviews where they advocate for mask-wearing and social distancing to continue in perpetuity even after COVID because of influenza, but they seem to assume it would only make sense if everyone wore a mask all the time. Influenza spreaders often spread the virus before they start to feel ill and think to put a mask on.
Given how much less dangerous influenza is I would expect even half measures to have a marked effect. We don't need to stamp it out entirely, we just need to curb it. The shot helps, but so would wearing masks when you're obviously sick.
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.
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.
I'm curious if that's just because zero flu cultures were ordered this year. People may have had the flu and covid, but they weren't testing for the flu.
My feeling from speaking to doctors (including an ENT specialist) is that while in our perception Covid eclipses everything else, for them it's just another infection on top of everything else.
So I would be very surprised (and see no indication) that doctors suddenly stopped doing standard diagnostics.
So I would be very surprised (and see no indication) that doctors suddenly stopped doing standard diagnostics.
Not the case at all. I don't have an exact number, but Alberta completed 300% more flu tests than the previous year.
https://globalnews.ca/news/7606557/alberta-2020-2021-flu-sea...
https://globalnews.ca/news/7606557/alberta-2020-2021-flu-sea...
Everyone presenting with flu-like symptoms at the clinics and hospitals that are part of the surveillance system get tested for about 30 pathogens. No one has stopped testing for flu.
Alberta has a population of 4 million people. 1,595 hospitalized and 41 deaths will simply strike many people as insignificant against that population, too small to justify lifestyle changes like wearing a mask. Considering how even during this time of COVID, many people have been observing restrictions only because they were warned the healthcare system might collapse (and thus affect them, too), not because they felt a drive to save every single life – and now that vaccines are being rolled out and the largest danger seems to have passed, masks are coming off left and right.
Just want to touch on the last sentence--putting a mask on once you feel sick can still lower the amount of people you give a virus to since you're lowering the number of days that you are easily transmitting.
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 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.
Why all the time? Can't we identify conditions where flu is most likely to spread and encourage mask wearing specifically in those situations? When things are back to normal I will probably still wear my mask on the subway for example, especially during rush hour in the winter. But walking around outside I would feel no need. I'm not sure exactly where the right balance would be as far as public willingness versus effectiveness in preventing spread, but it's definitely not going to be "everybody should wear masks all the time".
> The outstanding success of the last flu season let's us know that if we take it seriously
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?
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?
Let me give you the straight-forward answer from an epidemiological point of view (not an expert).
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.
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.
> 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.
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.
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.
> How do you explain the similar suppression in Sweden, Florida, Haiti, etc.?
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.
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.
> I would be very surprised if this did not result in a suppression of other pathogens, too.
>> 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.
>> 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.
I don't understand the way you are representing Sweden or how to weigh the point you're making with it. You're saying that, on one hand, SARS-CoV-2 (but mysteriously, not the other four endemic coronaviruses, which have identical communicability characteristics) managed to spread much more widely in part because "a different trade-off" was achieved, but on the other hand, that human behavior is an explainer for the suppression of all other aerosol-mediated respiratory pathogens.
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?
0: https://academic.oup.com/jid/article/212/11/1690/2911897
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?
0: https://academic.oup.com/jid/article/212/11/1690/2911897
Some cultures have normalized this (good hygiene and mask wearing when sick) since the 1917 pandemic.
I'm cautiously optimistic that it can take hold in the West this time around.
I'm cautiously optimistic that it can take hold in the West this time around.
Is there any evidence that respiratory viruses spread less readily in those countries in a regular year?
At least in part, yeah. I know I will. And every bit helps.
Do we really have to be so averse to death that we have to shut down life?
These sort of measures and proposals read as if you are talking about livestock, not humans.
These sort of measures and proposals read as if you are talking about livestock, not humans.
This is very interesting and has helped me understand something I hadn't realised before - if a disease is primarily spread by a small subset of the population(superspreaders), but you assume otherwise, it gets very hard to do statistics.
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)
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)
Just to clarify that both the fat-tailed distribution of R (most people don't infect anybody) and the low secondary attack rate (low infection in house holds) are also shared by Covid, and were one of the surprises early on.
This was a very intriguing and plausible-sounding hypothesis to read. Since this was 2008, are there good follow-up papers yet (or rebuttals)?
My thoughts exactly; we have had 13 years since this paper, what responses has it had?
As a non-expert I found it very interesting to see these parallels between influenza (even though partly conjectured) and SARS-Cov-2: The surprisingly low secondary attack rate of 20-30% and the fat-tailed distribution of R (this correlate of course to some extent), and a potentially mediating effect of Vitamin D.
Interesting hypothesis, and can be quite relevant today too!
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.