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No studies, which is shocking to me. It’s approved under EUA for a very limited set of immune deficiencies. EUA doesn’t allow it to be prescribed off label. It’s also around 10k per infusion. So, it’s very difficult to go for long covid. With that said, I’ve collected a dozen or so patient...

To me, this feels a little like the failed Rituximab trial. There are numerous credible N1s of LC patients cured with Pemgarda. There are several anecdotes out of UNC’a Long Covid Clinic alone. While I understand that N1s could be spurious (time heals, placebo, etc.), it just doesn’t feel that...

Could inhibition of PRDX be the cause of red blood deformability problems observed in ME/CFS? Per Grok, PRDX2 seems to be important for maintaining RBC deformability.

Reviving this thread as a result of the recent MIS-C COVID paper that found high TGF-Beta in COVID induced MIS-C. Perhaps TGf-Beta is also driving LC. Per-Grok: “Shedding of ACE2 reduces its activity, increasing angiotensin Il, which can stimulate TGF-beta production. If TGF-beta then further...

Is this good evidence that Long Covid is not a b-cell autoimmune disease given that it does not skew +-80% female?

So, I’ve been thinking a lot about LC’s relationship to ME/CFS. I have long covid, but not PEM. My guess is they are not the same disease, but LC is good at triggering ME/CFS. So, after COVID infection, one could have LC, LC and ME/CFS, or resolved LC with ongoing ME/CFS. If we assume this is...

Thank you, @Jonathan Edwards. I always enjoy reading your posts and greatly appreciate your feedback. As a lay person, it’s very interesting, and super helpful, to see how an expert in the field thinks through these things. Perhaps the narrower question I should have asked is this: Do we have...

My hypothesis is that Long Covid is caused by shedding of ACE2 receptors leading to prolonged down regulation of ACE2, disturbances in the RAAS system, inflammation via RAAS inflammatory pathways, and increases in ROS (which triggers ME/CFS in some, but not all LC patients). As a disclaimer...

Very unlikely. No diseases that features confirmed viral persistence look anything like LC.

I have two questions for anyone who might know the answer or have a deeper understanding of the science. First, after reading the paper thoroughly, I do not understand the use of SSRIs. The paper deals with peripheral serotonin and not brain serotonin. I can't find anything to suggest SSRIs...

So forgive me if this is a patently stupid question or has previously been discussed. I’ve looked and don’t see anything in archived posts here regarding the question I am about to ask below. Likewise, I can’t find any mention of related research with a google search. My question is this. Is...

Per Davis’ speech, not necessarily. If I recall correctly, there are two geographically distinct varieties associated with African Sleeping Sickness. One variety is easy to find. The other is extremely difficult to find.

Just thinking out loud, I wonder what happens to your gut microbiome when you are suddenly exposed to foreign food, water, and whatever else might impact the microbiome in a country like India.

Has anyone else noticed that a fair number of folks report travel to undeveloped countries before developing ME? It's entirely anecdotal, but this type of travel seems to pop up more than one would expect.