2024-03-22 General

I was out of town for a few days this week, so this post is short. I’ll catch up next week.


This paper from USA (2024-01-09) found that patients treated with selective serotonin reuptake inhibitors (SSRIs) had a 21-29% lower rate of Long COVID than controls. (The variability comes from which class of SSRIs — S1R agonists did better.)


In reading about the Thai Ducks Fighting Danger paper in Treatments below, I came across earlier work that is fascinating. It is well-described in a long thread (unrolled) (here’s the original thread on Twitter with very nice pictures, which don’t appear in the unrolled thread link) which itself refers to several papers.

In summary:

There are two different types of immunoglobulin gamma. 90% is what I will call the weak type and the other is called the strong type. The strong type is really strong and damaging, a ballistic missile to the weak type’s submachine guns. The strong type is more likely to get made when the immune system notices platelets which have antigens (foreign bodies) on their surfaces. (Possibly because it’s Really Bad if platelets get compromised.)

Sometimes people who get COVID have the cells which make platelets (bone marrow megakaryocytes) infected with SARS-CoV-2. That means that the platelets have COVID bits on their surface (which is a normal part of the immune system, cells routinely put stuff from inside on the outside). This alerts the immune system to make lots of the strong type of IgG. The strong IgG attacks, hard, any cell that is infected by SARS-CoV-2. Well, unfortunately, that’s lots of cells. Important cells that the people were kind of using. This is rough on the person. This paper found that people who have lots of the strong IgG get severe COVID, and people who only had weak IgG were fine.

This preprint from USA (2024-03-05) found that COVID-19 vaccination (and even infection) did not lead to the bone marrow making long-lived plasma cells — and long-lived plasma cells are at least part of what makes a vaccine effective for a long time. They found very different responses from influenza and tetanus: the ratio of not-long-lived to long-lived platelet cells was less than one for influenza and tetanus, and around THIRTY for SARS-CoV-2. (This paper from USA (2024-02-14) found the same thing.)


This study from Thailand (2024-03-14) was funded by “Thai Ducks Fighting Danger”, a social giving group. ❤️ 🦆

They found that treating COVID-19 mostly-vaccinated outpatients (between between October 1, 2021, and June 21, 2022) within 48 hours of symptoms with

  • fluvoxamine plus one of bromhexine or cyproheptadine


  • niclosamide plus bromhexine

recovered much much better than controls getting standard care — “completely eliminated the risk of clinical deterioration within the acute phase” — and had fewer Long COVID symptoms.

The different drugs do very different things:

  • Fluvoxamine is a selective serotonin reuptake inhibitor (SSRI), which removes serotonin.
  • Bromhexine inhibits TMPRSS2, which is one of two receptors that SARS-CoV-2 uses to get into the cell. (The other is ACE-2, which you’ve probably heard more about. Delta is better at using the TMPRSS2 pathway and Omicron is worse, which is part of why Delta was nastier.)
  • Cyproheptadine is a 5HT2 receptor antagonist; that reduces the effects of serotonin.
  • Niclosamide is an anti-worm medication which has several antiviral properties. Specifically, it blocks spike-induced cell fusion and syncytia (bunches of cells glomming together to form supercells).

In the paper’s discussion, the authors say that they think a lot of the utility of these medicines comes from dampening the immune system’s overreaction.

NB: There was also a fluvoxamine-only arm of the trial, and that group did better than the controls, but not as well as any of the combo therapy groups.

One of the authors wrote a long thread (original thread on Twitter but the pictures aren’t as important as the thread above under the Pathology heading) about the study. It explains why they chose the drugs they did. In part, serotonin is carried by platelets, and those platelets get attacked by strong IgG antibodies (see the first snippet in the Pathology section above). When the strong IgGs nuke the infected platelets, that releases a ton of serotonin into the blood stream. It turns out that serotonin is not just a mood regulator, it also helps in the formation of blood clots. (Uh-oh.) Serotonin also raises the amount of several interferons. (Uh-oh. Cytokine storm, anyone?)


This paper from Japan and Thailand (2024-03-21) found that there were significant differences in the amount of virus in the poo of people who had different (relatively recent) strains, and between symptomatic/asymptomatic patients.

They also saw different speeds of the virus showing up in the poo. 39% of patients had virus show up three days before symptom onset, while some people didn’t have virus show up until three days after symptom onset.

Mental Health

This paper (2024-03-21) found that people who had COVID-19 were 54% more likely than uninfected contemporary uninfected controls to have a mental health issue a year after infection. Patients who were hospitalized had slightly more than double the risk of contemporary controls. Unvaccinated or partially-vaccinated patients had a 64% higher risk than fully-vaccinated patients.