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That's interesting. The story from the other study is so nice though. Plenty of antibodies to other pathogens in CSF, but barely any to EBV, might suggest that primarily EBV-infected cells (that can't make EBV antibodies) are getting in. (Also Jonathan said B cells that make EBV antibodies...

Madelleine Müller - I Cant Run When I'm Dreaming (lyric video)

Could you quote the relevant part? I can only see the abstract.

Very cool, thanks.

Ok thanks that makes sense. Maybe still tough to squeeze through the tiles, but with millions of problematic B cells stopping, a few might make it through by chance. Five times bigger! I was imagining like 20% bigger.

Oh I was talking about MS where there's more reason to believe we'd actually find these B cells. Maybe something to look at in ME/CFS too though just in case.

I'm having trouble picturing how being bigger could make it easier to cross the BBB. Yep, that's the thread I linked.

I remember another thread with discussion about it being EBV infected B cells going into the brain and causing trouble. Would it not be trivial to look at the brain B cells post mortem to see if they all have EBV inside? Is it harder than I'm thinking to even find the B cells?

The main SNP here doesn't appear to be significant in the DecodeME data unfortunately. Data from DecodeME summary statistics. Converted rsID from this study to chromosome position ID using gnomAD. All DecodeME cases (p=.257) Females only, the way it was significant in this study (p=.428):

You got it. If they are hypothesizing about specific genes, they only have to adjust the p-value threshold for as many of these that they are interested in. They can even do a full GWAS on everything, strictly adjusting based on trying to find associations anywhere in the genome, and also do a...

I don't see any individual level data for illness duration in the study. Just a mean and range in Table 1. And I don't see anything about NK relationship to duration. Maybe it's from a talk?

It's a risk though. There might only have been significant hits just on the cusp of the threshold with the full sample. Reducing the sample size could lead to losing those findings. It might be better to put all the power possible in it while we've got it, and let the replication happen later.

Why do you refer to something like this as anti-inflammatory? You'd refer to something like TNF as inflammatory, right? In what way is this the opposite? It sounds like it's associated with neutrophils doing inflammation stuff. (Not that we know if the mutation increases or decreases whatever it...

Yep, here you go: I made it, but I'm not sure how useful this is because many participants are missing NK cell data at various timepoints. So some will include more later testing and some will include more testing in the middle of the trial.

Good idea to look at change in steps vs baseline NK count. I made a chart with the data from the supplementary files, keeping the same clinical improvement color label they use. Diff steps is the change in daily steps from the very start of the study to the very end. (I also flipped the axes...

Yes, the same two alleles that were risk alleles for ME/CFS in this other study: Human Leukocyte Antigen alleles associated with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): Fluge, Mella et al 2020 I feel like I must be missing something, because why was there never much...

Maybe. In theory this could mean people with ME/CFS have other HLA alleles that are good at presenting junk. But HLA alleles are different from regular DNA since there are very many possible HLA alleles, plus each person has several different alleles. So not having this gene doesn't necessarily...

Are you referring to a different gene in the main part of the study? This HLA part was looked at separately and they found another protective gene here (though they say they'll need to verify the association is correct).

Yeah, that could be good. They just have EBV, COVID, or other (columns are females, males, total, and total percent)

Well this specific allele from the study seems to protect against getting ME/CFS, which I don't think would fit with that. Maybe it's more like it's good at presenting a specific virus to T cells that is a common cause of ME/CFS and this fights the infection more quickly?