Talking sense about the Omicron variant

December 1, 2021 • 12:00 pm

Reader Tom sent me this 19½-minute video about Omicron from health science expert and nurse John Campbell, who’s apparently been dispensing sound information on the coronavirus for a long time. Tom said this:

Dr. John Campbell has been my go-to-guy for the past 14 months on a nearly daily basis.  He’s lucid, authoritative, clear, concise and engaging, just a superb source of reasonable advice.

When I asked for more information because Campbell’s Wikipedia bio was scanty, Tom added this:

He’s had a YouTube channel since 2008 and is an evidence-based medicine proponent to the bone.  His videos are daily, usually about 20 minutes long and shot in a spare room of his home.  Just him wielding a sharpie, an overhead camera, printed sheets of the day’s topic and a calm, no nonsense discussion delivered in a clipped English accent.  No histrionics.  Like visiting a well-loved teacher during office hours.

Now remember, we know very little about this virus—neither about its infectivity or its virulence (which really encompasses severity and spreadability).  So take this with a grain of salt. However, Campbell readily admits our ignorance while claiming, with support, that this variant will be the dominant strain throughout the world.

He does sound a note of hope, i.e., the vaccinated, when infected with Omicron, seem to get generally mild cases, and hypothesis that its spreadability is negatively correlated with how sick it makes peope.

John also gives us a pessimistic timeline for a vaccination (early to mid-2022). He summarizes where all the cases are (everywhere), and the mortality rate (thankfully, zero).  Remember, it’s early days.

15 thoughts on “Talking sense about the Omicron variant

  1. I have been following John Campbell as well for the last 15 months. Gives an excellent presentation with science based facts. He is easy on the ears, with good humor and honesty. He offers a lot of food for thought. There are several other interesting, science based, You Tube sites for Covid 19 information. Medcram, Ninja Nerd (don’t let the name fool you), and Vincent Racaniello’s various commentaries. No frills, just science.

  2. John Campbell is a steady hand at the helm. I’ve taken great comfort in his analysis of the COVID pandemic from the get go. He’s worth a watch.

  3. A worry that I have is that both the Delta and Omicron variants manage to co-exist in some fashion, where the Omicron cannot completely displace the Delta because they are different enough to escape immunity caused by the other. I am so accustomed to worrying these day that this seems a natural thing to put my worrying into.

  4. I’m not sure I buy the “can’t be good at everything” reasoning. Sure, the probability of being good at both transmissibility AND good at killing people would be less than either of those by itself but still, if you have lots of mutations involved (as is apparently the case here) why can’t some be for both traits?

    In any case, I hope Campbell is right. It would sure be nice to put the pandemic behind us.

    1. Generally speaking, when viruses are more virulent, in the sense of being more lethal, they don’t tend to spread as much because they kill people before they have as much of a chance to spread the viruses. Too much lethality is an evolutionary disadvantage in a virus.

      There are certainly things that can happen that “get around” this, like a long latency period before terminal illness, like with HIV (though that isn’t really very easy to spread), but it just tends to be the case that viruses that kill their hosts “aggressively” are less likely to spread as fast or as far. Especially when people are being watchful, the most lethal variants tend not to become the dominant ones.

      1. I understand the evolutionary notion that a more transmissible but less deadly variant will outcompete a more deadly and less transmissible version. I just don’t see what precludes a set of mutations that does both and, because of the higher transmissibility, comes to replace other variants that may be out there.

        1. I see. And certainly it could happen, of course, but the odds are much lower for getting both “abilities” than for getting either. And the “lethality leading to less transmission” principle does still hold, but it’s certainly not absolute, you’re quite right.

        2. I don’t know enough about precedent, but an example for both contagiousness and deadliness was the 1918 flu virus. It pretty quickly evolved to be just a regular flu virus, and as such it’s still in circulation.

          1. the 1918 flu virus. It pretty quickly evolved to be just a regular flu virus, and as such it’s still in circulation.

            Uh, the 1918 virus was an H1N1 influenza-A virus, and H1N1 influenza-A viruses are still circulating in both humans, swine and (I think) birds. But having two common characteristics (Haemagglutinin binding site type 1, neuraminidase binding site type 1) and being members of one family (“-A”), no more makes them the same virus than being mammals and having the characteristics of “flying” and “sticky-out ears” makes bats and “greater gliders” ( the same tetrapods.
            Off the top of my head, influenza A viruses have about 19 genes, with at least 8 common types in one gene, 11-plus in another gene, and I’ve no idea how many in the other 17(-odd). There is a lot of variation in the influenza-A family which is not captured in the “HnNm” classification.
            The original designation of the “Omicron” variant as B.1.1.529 may give a better reminder of this level of variation.

            Are there any geneticists in the house who can say whether or not viruses, when exploiting a new susceptible population, won’t (or don’t, or can’t) employ the relatively common eukaryotic trick of duplicating a gene and expressing both the original phenotype and the mutated genotype. Sure, later, when the competition is getting tighter, you’d expect the costs of copying 20 genes instead of 19 to have a selective cost, but when populations are expanding into a new vulnerable host, that cost isn’t so important as potentially doubling the target population.

        3. What follows is all speculative because very few people have had time to get seriously sick yet — the first cases of Omicron appear to have been in early November (retrospectively identified) according to John Campbell’s excellent and optimistic video above.

          However, what Campbell suggests (starting at 13:15) from his reading of the scientists is that Omicron may have put all its mutational “eggs” in the transmissibility basket and not in the virulence basket or the immune-escape basket.. Spike can be mutated in only so many ways, not infinitely, and many will be deleterious to the virus’s success. Again, for now this is speculation based on precedent but it does provide a possible mechanism for why this particular virus might have had to “choose” (with apologizes to our host for the teleologic reference) between transmissibility and dangerousness.

          (A pathogen with a larger genetic henhouse has many more mutational “eggs” and can distribute them into more baskets. Falciparum malaria remains unmatched in the trifecta of rapidly fatal disease even in the young and healthy, immune evasion, and highly efficient transmission, albeit requiring an intermediary mosquito.)

          The big caution about “mild disease” with Omicron is that almost all people diagnosed so far have been young with pre-existing immunity. (In Southern Africa this immunity comes mostly from prior infection with pre-Omicron variants and little from vaccination.) We have no idea yet what its effects will be on a spike-vaccinated older population (like the West) or a population with little vaccination or natural infection at all (pockets or large swathes of anti-vax resistance in a country where aggressive lock-downs kept infection rates low.)

        4. The problem is that it is difficulty in transmission that favors a reduction in virulence. In the case of humans and SARS-COVID-19, we are doing far too little to reduce transmission and thereby favor evolution of less virulence. There is no evolutionary reason in the current situation, given the ease of transmission, that both it and virulence cannot both increase.

  5. I’ve followed Cambell from the beginning as well. I agree with the general assessment that he’s a calm, rational, cautious voice during the pandemic.

    My only hesitation is that he seems to have been one of the voices keeping the ivermectin as a treatment for COVID concept alive, for many people.

    I’m not sure why he isn’t convinced by the problem of the ivermectin studies, that it seems really dubious as a treatment for COVID. As I recall he recently did a video with the suggestion that the Pfizer pill was essentially a type of ivermectin treatment, and that perhaps the downplaying of ivermectin itself might have roots in Big Pharma not being able to make money from it, rather than ivermectin not actually being efficacious for COVID.

    He’s been pushing Vitamin D for a long time.

    1. Agreed, that’s a major problem with John Campbell, his continued pushing of ivermectin against new evidence of flawed studies, even perhaps fraudulent studies. His promotion of Vitamin D is a little less problematic to me, hard to see the harm in that, although I will note that if you even dip your toes into the sorryantivax website or the Reddit pages devoted to this topic, you will see that almost all the cases documented there of unvaccinated folk dying of COVID involve rabid promotion of vitamin D and ivermectin as both preventative and cures, clearly quite ineffective, along with, of course, prayers.

      1. Hugh,

        Oh yeah, I’ve seen plenty of the sorryantivax stuff. It’s as you say: a sort of vitamins and ivermectin anti-advertisement.

        One signal coming out of all the sorryantivaxxer data is that having a goatee beard appears to be a significant comorbidity!

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