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Since when does "chronic inflammation" define ME/CFS?

Am I the only one skimming this and seeing they found lots of things, but little pathological insight?

I am struggling to sift out relevant/reliable information on ME etiology - especially regarding RBC deformability. If you are seeing valuable insights or data, would you mind pointing me to them?

Pending any such studies can we generalize that, for many cell types of interest to us, some HDAC inhibitor can significantly impact their predominant IFNs?

The paper says Type 1 IFN unaffected by HDAC blocker: but your thread Inhibition of Histone Deacetylation Induces Constitutive Derepression of the Beta Interferon Promoter disagrees?

You should be writing these papers - what a clear and crisp summary. I am very grateful - you have inspired me to now start a close reading of the paper and comments. Thanks again.

Seems like the 9 genes they identified ACADL, BRCA1, CFTR, COX10, HABP2, MFRP, PCLO, PRKN, and ZFPM2 do not show up in DecodeME. I WILL look at this (and the 24 pages of comments), but might you have a TLDR? Thanks so much for your help - all your hard efforts are obviously appreciated by...

I have spent an hour or two grappling with phasing and imputation, but realize the task is very large and complex. It just bothers me that most of the SNPs in the preprint are inferred by fiendish arithmetic. As you say, SequenceME will be a blessing. Is there currently ANY whole genome data...

Brilliant - I never would have found that. For example, if ALL pathological ME variants are absent on the UKB Axiom array, how sure can we be that imputation against the general population will cause them to be associated with pwME?

Re-reading the preprint paper, this non-scientist is struggling with how imputation was done (pooled cases+controls, versus separately ... if cases have unusual haplotypes surely separate imputation avoids forcing imputation from, essentially, population haplotypes ...). Is it possible to tell...

I find ChatGPT gives me a very useful leg-up with passages like those.

I really like the ideas in your post #161 - but what part does bone marrow play?

Thanks @forestglip I corrected that link. The 4511 controls study HLA -A, -C, -B, -DRB1, -DQB1 and -DPB1 allele and haplotype frequencies in 4514 healthy Norwegians is firewalled, but @Jonathan Edwards comment helps understand why DQB may be of more interest, and perhaps gives power advantages...

For example DecodeME found "A single class II HLA allele (HLADQA1*05:01) was associated with ME/CFS at genome-wide significance (p = 1.4 x 10-10; Fig. S7; Table S7). The frequency of HLA-DQA1*05:01 among cases (21.7%) was lower than among controls (23.2%) and so is predicted to protect against...

Forgive my ignorance, but why in Human Leukocyte Antigen alleles associated with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) did Fluge/Mella only "... obtained 2nd field resolution genotypes of ... and class II genes HLA -DRB1, -DQB1 and -DPB1...."? Have the -DRA, -DQA and -DPA...

Excuse my ignorance, but is there evidence that GWI and ME, despite having perhaps some similar symptoms, have similar etiologies?

Would it be fair to infer that there may not be much biology informing their paper?

Once AI can do the simple jumping frog puzzle I will pay attention to its thoughts (it's great for some things, but not thinking as yet).

I wasn't thinking about any immune role RBCs might have. I was more thinking if RBC deformability/etc has some merit in explaining ME/PEM, might bone marrow problems play into that.

Might RBCs be involved, perhaps linked also to ideas of RBC deformability/morphology/volume?