21 Comments

I would really like to see someone tackle, head-on, the tension between (1) keep your children masked indoors to protect them from common respiratory infections and (2) doing so reduces their overall immunity (incl possibly to COVID) and might leave them seriously vulnerable to childhood diseases if they first come into contact with them at older ages. It's all right there in the fifth paragraph, but it remains completely undiscussed.

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Exactly, you framed my above questions in fewer words.

It's possibly a poor analogy, but we (mostly in the US) spent close to 2 decades delaying introduction of peanuts to nursing mothers, babies, and toddlers, expecting to reduce severe anaphylaxis reactions to peanut allergies.

We slowly came to realize that all we did was create a larger pool of children predisposed to having peanut allergies.

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I would also love to read about that! I'm very Covid cautious but worry that my preschooler may not be getting enough exposure to other things to build immunity.

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I have a couple of comments also: I think going forward we need to move to wearing masks when we are unwell, to try to limit the spread of viral illnesses, as I do think it helps our immune systems to fight off some viruses, or re-activate our immunity from vaccination, but let's try not to spread it to everyone, especially more susceptible hosts.

Second point: we need to remind the public that store bough disinfectants that kill 99.9% of cold and flu viruses are fine on RSV, Influenza, SARS-CoV-2, Human Metapneumovirus, parainfluenza...but will not be effective on Rhinovirus, Enterovirus, Parechovirus and other small, non-enveloped viruses. I fear we trust our disinfectants too much without recognizing the limitations against some of these hardy, surface-surviving small, non-enveloped viruses.

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Interesting write-up. I noticed that Dr. Sivasankar removed his tweet, any idea why?

There were 3 areas of this post I'd enjoy further analysis/discussion:

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KJ: "The measures we all took to slow the spread of SARS-CoV-2 also worked on all the other viruses."

That is one hypothesis, but I believe may be falsified by the fact that in places where the measures were not adopted, or, adopted at far lower rates, had no different outcomes than places with strict adoption.

The flu, for example, also disappeared in countries like Sweden, Norway, Denmark, Finland in 2020 the same as anywhere else - despite these countries sending their kids back to school the spring of 2020 and mostly remaining open throughout the entire pandemic. All of the Nordic countries had among the lowest masking rates of the entire world as well and masking children was far rarer than the rest of the world.

Similar examples could be made of South Dakota, Iowa, Florida, and other states which relaxed measures relative to neighboring states and didn't have any different outcome.

What are some alternative hypotheses which could explain why SARS-COV2 dominated while other viruses retreated regardless of NPI? The leading argument I have heard is so-called "Viral Interference" - that just as the various strains of Covid19 vie to become dominant, might other ILI respiratory viruses also compete at a macro level? That might explain why for two years the forecasted "twindemic" scenario didn't occur.

What are your thoughts on this theory? Could it help explain why Flu retreated in areas with relaxed social distancing, children in school, and low mask usage? Are there other theories?

I can't seem to find much in the literature on this prior to 2020. (Tenuous examples like this https://www.pnas.org/doi/10.1073/pnas.1911083116 and https://academic.oup.com/jid/article/212/11/1690/2911897 are what I come up with).

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KJ: "The drawback is that the population immunity normally maintained through regular cold and flu seasons eroded, leaving more people (especially kids) without recent immunity. Experts have been warning that this creates the conditions for a severe respiratory virus season (especially flu)."

Would this give support back to the "hygiene hypothesis" - that routine exposure to germs, dirt, viruses etc in children helps build their immune system? That a disruption in the background immunity building to avoid one pathogen might leave us more vulnerable other pathogens and backfire?

Just as we recently came to understand our avoidance of potential allergens (notably peanuts) in recent decades wound up creating more children with severe allergic reactions, could avoidance of viruses inadvertently lead to a worse long-term outcome? (or perhaps a net zero outcome).

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KJ: "Waves of AFM appear every two years, a trend that epidemiologists first noticed in 2014. The 2020 wave was skipped, likely because the measures taken to prevent COVID-19 also prevented EV-D68 from circulating."

In the "off" years of 2015, 2017, 2019, were EV-D68 infections also down as well? (I assume they were).

Could it be that whatever caused EV-D68 to recede in those years may also have caused it to recede in 2020 as well? The "it comes every 2 years" theory has such a short history of observation it seems prudent to understand why it was skipping some years and not others. What are the plausible theories to explain the bi-annual gaps? (Could the earlier mentioned viral interference be at play?)

The CDC and other literature notes that DV-D68 is one of several viruses linked to rarely triggering AFM, so AFM seems to fall under the umbrella of "post viral syndrome" - rare, long-term outcomes following a viral or bacterial infection (e.g., PANDAS from Strep for children). Considering this, would children who presented the clinically as having limb weakness following a Covid-19 infection be counted as having AFM or Long Covid in 2020-2021? If 40 children had limb weakness post Covid 19 and we classified as Long Covid instead of AFM, might that also explain the skip in 2020 or 2021? Complete speculation but seems worth considering.

(I realize that the incidence rate of AFM is nearly infinitesimally small against the population so it could simply be we are seeing patterns out of randomness because I brains evolved to see patterns)

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Thank you for including AFM! As a family affected in the 2016 outbreak, I’m very concerned.

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founding

Thank you very timely. Question does the same basic pattern apply to adults who are getting back into the swing "social interactions" from workplace to back to school night to bowling.

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Correcting your heading from "may be" to "ARE", Dr. Kat. :-) Here in KC, we are also seeing unusually high office visit numbers of ILI and other respiratory-like illnesses. We are preparing our staff for an expected illness boom, and getting stocked up with flu and covid shots for anyone who wants one!

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To summarise, because we successfully protected our kids from viruses, they are now more at risk from viruses.

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I think one issue driving parents to not bother about proactively protecting their children by using masks, etc., is the prevailing feeling that it’s okay for kids to get colds, etc. because that’s life…and, I got it when I was a kid and I am okay. This is cultural and very hard to change.

From a long time school volunteer

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Do we have any information on when the bivalent COVID booster will be available for the under-12 crowd?

It is so frustrating to see this pattern repeat, where there is a potentially protective vaccine that is out of reach for kids, and we just have to send them out into the world with suboptimal protection. AGAIN.

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Sep 25, 2022·edited Sep 27, 2022

Question: Paxlovid rebound.

I had the vaccine and all the boosters available at the time, then caught COVID. Because of diabetes and asthma I chose to take Paxlovid (which was god-awful). Five days later I tested negative and then again tested negative another time after that. During COVID I had very mild symptoms (I had a cold that was worse 6 months prior). Three days after I tested negative the second time I again tested positive. No symptoms. Before testing I had been around people all day in close quarters in a vehicle, even hugged a couple of elderly ladies and called these people because I thought I might have exposed them. Nobody 3 days later tested positive that I was in close contact with 8 people, including the 5 people I was in a car with for at least 2 hours. Everything I have read says there is not enough data to determine how long some people need to take Paxlovid. I took it for the entire 5 days. I have not yet gotten back my PCR test yet so I am still in quarantine. but feel fine. Please explain the mechanics of this. If you have already, please give me a link of that note. I have followed your newsletters throughout COVID, found them informative and appreciate all the hard work you do. Thanks in advance.

Update: I got a call from my doctor today 5 days after positive and he said I have long COVID and its rare, but he told me not to test again unless I have symptoms for the next 90 days, as he said I could get a spurious result. That I should mask and quarantine for an additional 5 days just to be safe and the PCR test and other antibody tests (from Labcorp) were not necessary. He said this was a "quirky" thing about COVID. It still leaves me wondering and puzzled about this occurrence, as I stated before I would like to understand the mechanics of this.

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Slightly off topic, but what is the rationale for the bivalent vaccine containing mRNA encoding the spike protein of the ancestral strain? Is it because it might be used for unvaccinated individuals? Is there a reasonable concern of immune imprinting when it's included in one's 3rd, 4th, or 5th vaccination? Thank you!

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Imagine you're given two words, and you want to make as many new words out of the letters from one or both of those words as possible. You want those two starting words to have as few shared letters as possible.

That's how we should think about our immune systems responding to vaccines. It's not about variants (words) but covering as many mutations and reversions (letters) as possible. There are lots of shared mutations across variants! This is an important fact, given that the virus has by now probably made hundreds of trillions of copies of itself but keeps recycling a lot of the same mutations.

https://covariants.org/shared-mutations

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Thanks to Hypervaxxed and KB for their clarifications on this topic. Helped me make the decision to get the bivalent this week (especially as we see new Omicrons entering the playing field). Until we have a vaccine that prevents getting infected in the first place and prevents transmission, it seems like a low-risk strategy may be: Vaccines to reduce chance of severe disease if infected and properly-worn N95s when inside public places or outside if crowded and vigorous handwashing/sanitizer (just in case!). But I sure miss my conferences; big crowded rooms with <20% masked. That strategy is informed by my personal risk tolerance; I don't give people the evil eye if they're not masked and I am blessed to live in a community where they don't when I do.

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If OAS were a problem, it would have reared its head during the Delta wave, and it...didn't. Omicron has so many mutations compared to the original Wuhan virus that OAS stops being a problem.

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It's "lurking" in the sense that evolution doesn't have any particular direction. It's just random transcription errors. Having two very different variants (Wuhan and the latest shiny new model) covers a large range of mutations and reversions.

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I have a question about anti-bodies. When we get vaccinated we develop a high number of antibodies that wanes over time. If we get exposed to COVID during a time that our antibodies protect us from infection, does the antibody count go back up to vaccinated levels?

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Thank you for doing your part! I actually think that people who participate in clinical trials should be afforded a military rank, with all the attendant benefits for the rest of their lives

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KB - When do you get unblinded?

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