Covid-19 will be one more disease among many, and life will be marginally worse, but by about April you shouldn’t act substantially differently than if it no longer existed.

This seems quite bold given our history of variants emerging. And if Omicron infects billions, then prima facie there's great opportunity for mutation. I'd be interested to hear your credence in the following proposition:

From 1 May 2021 to 1 Jan 2030, Zvi won't act substantially differently due to risk of SARS-CoV-2 infection.

Additionally, "one more disease among many" suggests (to me) that it won't cause 100K+ more deaths in the following few years, which also seems bold. [edit: American deaths, see replies for more]

Could you do readers an enormous favor and put references in when you say stuff like this:

"Vitamin D and Zinc, and if possible Fluvoxamine, are worth it if you get infected, also Vitamin D is worth taking now anyway (I take 5k IUs/day)."

1. First two shots don’t protect against infection, boosters do somewhat (60%?).

I'm guessing you mean "first shots obtained in spring or summer are likely to have declined by now"? Or do you mean the third shot gives you more immunity than you ever had with only 2?

I'm skimmed mostly all of your covid posts, so in theory this shouldn't really be teaching me anything new, but I found it to be a very useful compilation. Thank you!

Budesonide?

I was wondering if you had updated your thoughts on how much viral loads matter since your April 2020 post on it. I live in a co-living space of over 60 people with poor ventilation. I'm wondering if that means I should worry about getting covid more than the average healthy 30 year old man.

Also, I wanted to more enthusiastically thank you for your feedback on my fantasy sports poker card game in July.  You saved me a lot of time! I decided not to continue doing it.

What form of zinc are you suggesting people take?

Omnicron probably milder than Delta (~50%) so baseline IFR likely ~0.3% unless hospitals overload, lower for vaccinated or reinfected.

Protection against hospitalization is probably something like 80%, with likely additional protection above that against severe disease, and then even more protection against death.

From some quick googling vaccination seems to provides about 10x reduction in IFR, so we are looking at ~ 0.03% IFR for the vaccinated, or about ~ 0.14% overall (0.6 * 0.03 + 0.4 * 0.3), and in practice perhaps lower if we factor in natural immunity, so getting close to the ~0.1% IFR of seasonal flu (although the latter does have a lower vaccination rate).

Omnicron of course is still higher overall impact, due to the higher case loads. But overall this seems encouraging in directionality.

The 1918 H1N1 spanish flu variant had an initial IFR in the estimated 5% to 10% range, and killed estimated 10x more people than covid has so far, but it's modern seasonal derivatives are far less deadly.

Zvi, what are the chances that Paxlovid ends up having way more side-effects than the trials showed? I heard David Friedberg on the all-in podcast mention that he was pretty nervous about it because the drug messed with some pretty fundamental biological machinery, and that under non-covid circumstances it would be tested for a lot longer. I don't doubt that for people that end up at the ICU the benefits will overwhelm whatever side-effects end up happening, but how would the risk evaluation go for people with mild or mild-to-severe illness?

There is a War, and the WHO, FDA and CDC, and most similar agencies abroad, and most elected officials, are not on our side of it. Instead they focus mostly on getting in the way, protecting their power and seeking to avoid blame on a two week time horizon.

Can I get an explanation of this? This is my first time reading about Covid on LessWrong (I'm new). My general impression (with no investigation or research) was that the WHO and CDC were doing a reasonable job in trying to figure out what was going on and giving reasonable advice on how to reduce the negative impacts of Covid. Am I under the wrong impression?

Curated. This is another unusual curation, in that this is not a timeless post, but it does just seem pretty important for many readers.

I do encourage people to check claims for themselves and comment with counterarguments or additional research where appropriate.

When I edited to fix an error in #9 it messed up the numbering system. Mods, please either fix or simply reimport. I continue to ask that this be fixed so we can start lists with numbers other than #1.

There might be another strain in the future. I don’t know how likely this is, but that’s the most likely way that things ‘don’t mostly end’ after this wave

I agree, and I also don't really have great mental handles to model this, but this seems like the most consequential question to predict post-Omicron life. My two biggest surprises of the pandemic have been Delta and Omicron, so sorting this out feels like a high VOI investment.

Here's a messy brain dump on this, mostly I'm just looking for a better framework for thinking about this.

1. The amount of transmission obviously matters, since more generations provide more opportunities for mutation.  All else equal, VOCs are more likely to arise where cases are high.
2. Is a partially vaccinated population more likely to generate VOCs? Either in the sense of a large number of single dosed people, or a large proportion unvaccinated, or some complex interaction of the two?
3. If mutation and selection is happening within an immunocompromised individual (as opposed to gradually accumulating in a population), does this imply regions with high HIV-AIDS rates are most likely to produce VOCs? Are there other clusters of immunocompromised people, or are they fairly evenly distributed?
4. The two VOC (Beta and Omicron) with the most immune evasion arose (or were at least first detected) in South Africa. Is that a coincidence? Is the presence of a BSL-4 (the only such institution south of Gabon)? Origin vs detection is confounded by the relative abundance of sequencing resources in SA vs the rest of Africa, which makes detection in SA quite likely even if VOCs emerge elsewhere, but the pattern of spread of both Beta and Omicron are more consistent with SA origin.
5. Is any of this modifiable through policy decisions? The WHO is urging wealthy countries to forgo boosters in favour of distributing doses to the developing world, which is on-brand lunatic messaging given current events, but post-Omicron wave could this actually be good policy? Maybe this depends on sorting out some of the above?

Six Feet Is An Arbitrary Number. There’s still nothing better than an inverse square law, so by default I presume 12 feet is a quarter of the risk of 6 feet, and 3 feet is double the risk, there is no magic number.

Should this say that 3 feet is quadruple the risk of 6 feet, if we're assuming an inverse square law?

Vaccination with three doses is protective against infection by Omicron, but less protective than vaccines were against Delta. As a rule of thumb I am currently acting as if a booster shot is something like 60%-70% protective against infection but I don’t have confidence in that number. The main protection is still against severe disease, hospitalization and death.

Two questions about this:

1. Do you mean that a booster is 60-70% effective relative to being "fully" vaccinated but not boosted, or do you mean that being boosted is 60-70% effective relative to being unvaccinated?
2. How did you reach this conclusion? Based on the Pfizer press release, I had been treating being boosted as 95% effective (relative to being unvaccinated) since the level of neutralizing antibodies against Omicron with 3 doses was the same as the level against original Covid with 2 doses, and 2 doses were 95% effective against original.

Typo:

Much of infectiousness proceeds symptoms.

Precedes?

"The risks of Covid-19 prevented by vaccination greatly exceed the risks of vaccination."

Is this true across all age groups?  I've been getting PO'ed at radio ads in NY encouraging moms to get their 3 year olds vaccinated.  But maybe this is my mistake.  

Regarding long COVID: Zvi, does your model above incorporate the following findings (published after your original deep dive in Sept)? (If anyone other than Zvi has thoughts on how these affect the model laid out above, would be curious to hear your thoughts as well.)

• 9/29/21 NPR article recapping a study from around that time
  • Affects over 1/3 of COVID sufferers, 2x as high as for flu:
    • "In the study published Tuesday in the journal PLOS Medicine, researchers found that about 36% of those studied still reported COVID-like symptoms three and six months after diagnosis. Most previous studies have estimated lingering post-COVID symptoms in 10% to 30% of patients.
    • ...Although long COVID is poorly defined, the researchers looked at such symptoms as chest/throat pain, abnormal breathing, abdominal symptoms, fatigue, depression, headaches, cognitive dysfunction and muscle pain.
    • ... the new study concludes that the chances of getting COVID-19 symptoms months after the acute stage of the illness was more than twice as high as for influenza."
  • Other points to consider:
    • "The Oxford-led team also found that people who had more severe COVID-19 illness were more likely to get long COVID. Likewise, female and young adult patients also had an elevated risk for the long-term symptoms, but the authors of the study found no difference between white and nonwhite patients."
• 11/24/21 Reuters article noting that "COVID-19 vaccines are highly effective in protecting against serious illness, but they do not protect against "long COVID" in people who become infected despite vaccination"
  • (However, both the article and the study it cites note that vaccines are protective against long COVID to the extent that they prevent infection in the first place.)

And thank you for this post and everything you've written throughout the pandemic!

Is there a good write up of the case against rapid tests? I see Tom Frieden’s statement that rapid tests don’t correlate with infectivity, but I can’t imagine what that’s based on

In other words, there’s got to be a good reason why so many smart people oppose using rapid tests to make isolation decisions

I am confused about why it's better to get Omicron later rather than sooner. I understand that avoiding overloaded hospitals is a good idea, but the reports from people who have Omicron (understanding that first-hand reports are created by people well enough to report and/or by bad actors) suggest that getting Omicron right now is equivalent to a nasty cold. 

Even the data suggests that getting Omicron right now is much less likely to lead to hospitalization, regardless of whether you feel chipper enough to tweet about it.  

So... why do you assume that catching Omicron in March instead of right now will lead to better outcomes on the individual and/or public health level? Omicron might not be the dominant variant in March, after all, and getting immunity now could be a smart move. The equation changes if you have comorbidities, of course, so I may only be speaking for my own long-term health goals here.

(yes I have read Tyler Cowen's post about this)

There are two points numbered "27", one above and one below "Next, testing and isolation."

53. Taking action to ‘stop the spread’ mostly no longer makes sense.

From the context, it sounds like this refers to the time after the current wave is over, but if you don't consider context, it could easily be interpreted to apply already. 

I am very suspicious about statement that I cannot avoid getting omicron, unless I take extreme measures. Why ? Because I have heard the same about delta and it was false.

I have a friend in Germany, she teaches at school, where rapid antigen testing 3 times a week prevented the school transmissions. They know it, because if a child is flagged as a contact, they test them daily, so they have this feedback.

I pulled away my children (3 yo and 6 yo) from school and kindergarten and they did not get delta. The delta peak in our town did happen already. The kids also did not go indoors apart from our home and the granparents. Are these extreme measures ? In some sense yes, because it put a great strain on a relationship with my partner, I can feel he is dissapointed in me in a last few days. But from what I was told before about the terrible delta, I thought this might be insufficient ! We do not mask at the corridor in our block of flats, which contains 8 other families. Children can play outdoors with other kids. My partner did go shopping masked by FFP2, I went to work masked by FFP2 in the corridors.

My experience is, that preventative measures work. But if you believe, there is no point trying to avoid infection, you will get infected.

I presume 12 feet is a quarter of the risk of 6 feet [...] there is no magic number

My intuitive oversimplified model of this has been analogous to the direct sound vs reverberant sound in acoustics (in slow motion). 

I'd expect the risk from direct viruses to follow the inverse square law (at least to the extent that the risk is linear to the expected number of viruses around you, which can't be true for high risks). And maybe be even be reduced by cloth masks which stop big droplets (?).

But the reverberant viruses are supposed to be the main drivers of the pandemic, right? And those don't care about distance for small enough rooms where virosols (heh) have more than enough time to travel everywhere before falling down. This is where N95s and ventilation become crucial, but distancing not so much.

In this model, there is a special distance, a "critical distance" (which depends on the context, masking, etc), after which the direct viruses are as important as the virosols and extra distancing starts not mattering. 

Is my intuitive model nonsense?

Support Longevity Research. If you think that people dying is bad, maybe we should do something about it.

But not gain of function research?

A negative rapid test should be necessary before ending isolation. The CDC’s new guidelines don’t say this but this seems overdetermined and obvious to me. If you care about not being infectious, you should check on that before exposing others.

How common are false positives after infection?

Eg the CDC says that: 

Recovered patients: Patients who have recovered from COVID-19 can continue to have detectable SARS-CoV-2 RNA in upper respiratory specimens for up to 3 months after illness onset. However, replication-competent virus has not been reliably recovered from such patients, and they are not likely infectious.

Which suggests they might be not that uncommon.

UTSouthwesterner Medical Center says that (the CDC says something similar):

How can a patient have a positive PCR test but not be infectious?

Reverse transcriptase-quantitative polymerase chain reaction (RT-qPCR) is the primary method used to diagnose SARS-CoV-2 infection and many other viruses. The test works by creating copies of viral genetic material in respiratory samples over many cycles. A single copy of viral RNA can be amplified to more than 2 trillion copies during a typical 40-cycle testing protocol. Amplification of genomic sequence is measured in cycle thresholds (Ct) and the Ct values correlate with whether a sample contains infectious virus particles. If the viral RNA is detected after just a few amplification cycles (i.e. at a low Ct value), that means high RNA levels are present and thus more viable virus; however, because this test is designed to be a sensitive diagnostic tool (not for monitoring disease progression), a very high Ct value (low RNA level) is set as a positive range cutoff. This means that very low levels of the RNA or viral genomic fragments can test “positive” for months after the acute infection but are not associated with live virus. This detection issue is common for other RNA viruses.

Which suggests to me that PCR testing might be prone to false positive after an infection, but does not clarify to me if Rapid Antigen Tests are also prone to false positives.

My guess is that false positives in the Rapid Antigen Test are uncommon, since the proposed causal mechanism for why PCRs give false positives is because of the viral load amplification, which does not happen with Rapid Antigen Tests.

The key question: should I end isolation after 10 days regardless of rapid antigen test result?

I've asked https://www.lesswrong.com/users/connor_flexman [LW · GW], a person who has previously estimated the number of expected days of life lost from covid (see for example https://www.lesswrong.com/posts/GzzJZmqxcqg5KFf8r/covid-and-the-holidays [LW · GW]), how to update his estimates for the assumption that 100% of covid is omicron. On december 27, he told me that covid means 10 expected weeks of life lost for an average 30 to 50 y.o. person. And that to update https://microcovid.org estimates, you should multiply by 3.5 because omicron is more infectious and divide by 3 if you've had a booster.

Note that this post mostly does not justify and explain its statements. I document my thinking, sources and analysis extensively elsewhere, little of this should be new.

This is my first encounter with your writing, could you or someone else recommend a starting point that does justify and explain these statements?

I write to commend you on one of the more thoughtful blogs on COVID-19 that I have read. I've been modeling, and writing about, SARS-CoV-2 since March of 2020, and following the literature closely. Your assessment and practical advice seem spot on. Thank you.

I think my only criticism is your one sentence polemic about the FDA, the CDC, and WHO. While I don't know anyone at the WHO, I have many colleagues at both the FDA and the CDC. The FDA and the CDC respect science, respect data, and respect regulations. They were villified under the previous administration, and are struggling to return to their scientific / public health roots under the current administration. I can confirm that the CDC website is again a source of useful information and guidance. I'm disappointed that it took the FDA so long to get vaccines into children. However, I also respect both agencies for following the rules, even if some of the rules are now outdated or need revision in the face of a public health crisis. An anti-vax / mask denying / "no worse than the flu" person could cherry pick this comment to discredit their efforts to promote vaccines, treatments, and public health. You might consider toning it down.

Having said that (more as an afterthought than anything else), I'll send people to this page for clearly stated assessment and recommendations that are (otherwise) consistent with the ever emerging data.  

You are forgetting declining immunity. Next winter may very well have a similar wave again. In fact this is imho the central scenario (60%ish probability). Quite possibly with multiple strains.

I agree with most of your post, but this looks like wishful thinking to me.

Also, individual prevention should be way easier than you make it out to be. Wear a well fitting N95 or better mask when meeting people and you are mostly done if you live alone or with compliant housemates. Just look at Covid stations in hospitals. Staff there is wearing mostly N95, often poorly fitting and even they do not get infected on the first day (or week) despite MUCH more exposure than we will ever get. Masks work! Masks not working in the general population is a compliance problem, not a technical problem.