> The big story last year was that cases of/deaths from influenza dropped worldwide[1]. There's a huge difference between "influenza plummeted worldwide" and "

> The big story last year was that cases of/deaths from influenza dropped worldwide[1]. There's a huge difference between "influenza plummeted worldwide" and "influenza plummeted worldwide as a direct result of school closures [or lockdowns, physical distancing, and universal masking]". Influenza did plummet worldwide. Indeed, it did so even in places that didn't go to nearly the same extent as the US did as far as school closures and the like. That should already hint at you that it's not actually related to what we did intervention-wise (which also makes sense given that everything we did was ineffective at slowing the spread of COVID more than a marginal amount [granted, SARS-2 spreads more easily than Influenza so it's theoretically possible the COVID measures were completely ineffective for COVID yet were completely effective for Influenza, but seems farfetched]) To me the most plausible explanation is that of viral interference: https://pubmed.ncbi.nlm.nih.gov/30950360/ https://pubmed.ncbi.nlm.nih.gov/30950360/ > Since the interferon system can control most, if not all, virus infections in the absence of adaptive immunity, it was proposed that viral induction of a nonspecific localized temporary state of immunity may provide a strategy to control viral infections. Briefly, infection with a virus causes one's cellular hackles to get raised, so to speak. That is to say, that infection with virus A leads to a ramp-up in innate immunity, particularly cell-mediated innate immunity, which decreases the probability of being infected by virus B in the ensuing days/weeks. The paper I linked is about leveraging that intentionally, but obviously it's a mechanism that occurs naturally as well. This next point is orthogonal to our discussion but I'd be remiss if I didn't mention that SARS-2 is, in a sense, actually the ideal candidate for intentional exploitation of viral interference, given how readily it infects human cells and how in large swaths of the population it is very non-threatening (and yes, in a small proportion of the population it is very threatening) -- So to tie it back to the Influenza dropping, I suspect that viral interference was quite significant, and that altered social interactions accounted for a big chunk of it as well. Specifically, it seems like social networks got much more "local". There was still people going out and doing stuff, but overall the average person was significantly less likely to visit extended family, attend large events, etc. This is somewhat related to the lockdowns/forced shuttering of businesses, but I think a lot of it was broader than that as well. --- > Can you link to those studies [regarding influenza and school closures]? I'll start with one review that does seem to suggest a benefit in school closures for Influenza: https://bmjopen.bmj.com/content/3/2/e002149.short https://bmjopen.bmj.com/content/3/2/e002149.short. It has the usual problems associative studies do, but in this case specifically the confound of regression to the mean is incredibly great. They mention as such in the results: > However, as schools often closed late in the outbreak or other interventions were used concurrently, it was sometimes unclear how much school closure contributed to the reductions in incidence. Here's one from Hong Kong. I really like their discussion because it points out just how difficult it is to actually show a link, given the way epidemic curves naturally rise and fall and the delayed natural of intervention impact: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2609897/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2609897/ > Although we can only speculate, given the limitations of an uncontrolled natural experiment on the population level, routine surveillance data did not detect a large effect from the school closures. In particular, we noted a decline in laboratory isolations of influenza viruses that preceded the intervention and the lack of association between school closures and Rt. In fact, sentinel data may not accurately represent the incidence of influenza in the underlying population because, for example, other cocirculating upper respiratory viruses contribute to overall influenza-like illness consultation rates. Laboratory data, however, should be less affected, and extra testing in response to the heightened awareness of influenza activity might have artifactually lowered the positivity rate. The epidemic curves generated from the surveillance data showed a decline in cases that may have naturally concluded without any intervention. We note the difficulty of making inferences directly from changes in epidemic curves because changes in the epidemic curve may lag behind changes in the underlying transmission dynamics by at least 1 serial interval, as has previously been shown for severe acute respiratory syndrome - This next one is more about the ethics, but I think the abstract is pretty sensible: "Mitigating Pandemic Influenza: The Ethics of Implementing a School Closure Policy" - https://journals.lww.com/jphmp/Abstract/2008/07000/Mitigating_Pandemic_Influenza__The_Ethics_of.11.aspx https://journals.lww.com/jphmp/Abstract/2008/07000/Mitigatin... > Pandemic influenza response plans have placed a significant emphasis on school closures as a community mitigation strategy. However, school closures raise serious ethical concerns, many of which have been largely overlooked. First, evidence of this intervention's efficacy has not yet been firmly established, calling into question whether it will be useful against the threat. Second, school closures have the potential to create serious adverse consequences, which will disproportionately affect vulnerable populations. Thus, policy makers should focus on gathering more evidence about the efficacy of school closures and on strengthening communication and transparency about the strengths and weaknesses of any school-closure plan that they decide to adopt.