2021-03-08 General


A preprint says that people who had B.1.351 had antibodies that worked well against COVID Classic and also against P.1. This is outstanding news — it means that the counter-B.1.351 boosters being developed will work against the scaries!

There is yet another study which says that, while the effectiveness of mRNA vaccines (Pfizer in this case) is reduced against various variants, it is should still be good enough.

This paper finds that vaccination with Moderna should be fine against B.1.1.7, but that B.1.351 has significantly increased resistance. (It does not render a judgement on whether the Moderna vax is good enough or not.) The paper also shows that many monoclonal antibodies (e.g. bamlanivimab, casirivimab) have markedly reduced effectiveness against B.1.1.7 and B.1.351. Convalescent plasma from COVID Classic patients had good effectiveness against B.1.1.7 and reduced effectiveness against B.1.351.

And here’s a popular press (San Diego Union Tribune) article which talks about how the vaccines work well enough against the variants.


This study says that there were only 16 cases (0.025%) of anaphylaxis among ~65,000 who got mRNA vaccines, and all recovered.

This preprint says that a second dose of an mRNA vax isn’t much use for people who have had COVID-19 already. It’s not harmful, but just doesn’t do much. (One dose, however, is a good idea.


This thread lays out an argument that COVID-19 will become endemic by analogy with other coronaviruses, the “common cold” viruses. They point out that we ALL get the common-cold-coronaviruses as kids, and that they can be deadly to adults, especially older ones. We don’t think of them as deadly because we all have antibodies to them now.

This opinion article in Nature suggests that right after a virus jump species, it mutates relatively rapidly as it adapts to its host, but once it figures the host out, it basically stops mutating: it finds a local maximum and stops there.

Disease Exacerbators

This paper found a high correlation between COVID-19 infection rates and pollen! It explains the possible connection: “Pollen exposure weakens the immunity against certain seasonal respiratory viruses by diminishing the antiviral interferon response…we suggest wide dissemination of pollen‚ąívirus coexposure information to encourage high-risk individuals to wear particle filter masks during high springtime pollen concentrations.”

That does not make sense to me: we saw greatly increased rates in the fall/winter, when pollen counts would have been greatly reduced.

This article from the US CDC shows that being obese is a significant risk factor for requiring a ventilator (IMV in the chart below) and/or dying from COVID-19.


This preprint followed patients and determined that Long COVID was correlated to being female, severity of illness, and weaker antibody responses.


In this paper in Nature, the authors knocked out (disabled) genes, one at a time, of 20,000 genes in the human genome. They then introduced COVID-19, and saw which cells died and which lived. Usually, the cells died, but they found 30 genes where cells lived when that gene was knocked out. This means they could figure out which proteins COVID-19 needed in order to infect the cells.

Great news: there are already some drugs which can regulate some of the critical genes, including Amlodipine, Tamoxifen, and Ilomastat. They dosed cells with those drugs and then introduced COVID-19, which didn’t infect the cells. Awesome! Here’s a popular-press explanation.

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