Do you mind listing what those 3 studies were? The first thing that comes to mind to check is whether all of them were done after Covid started.
This thread's study, plus the following two:
Plasma proteomic profiling suggests an association between antigen driven clonal B cell expansion and ME/CFS, 2020, Lipkin et al
IGHV3-23/30 and immunoglobulin kappa variable region 3–11 were significantly associated with ME/CFS without sr-IBS.
Skewing of the B cell receptor repertoire in myalgic encephalomyelitis/chronic fatigue syndrome, 2021, Sato et al
By applying a next-generation sequencing to determine the clone-based IGHV/IGHD/IGHJ repertoires, we revealed a biased usage of several IGHV genes in peripheral blood B cells from ME/CFS patients. Results of receiver operating characteristic (ROC) analysis further indicated a possibility of distinguishing patients from healthy controls, based on the skewed B cell repertoire. Meanwhile, B cell clones using IGHV3-30 and IGHV3-30-3 genes were more frequent in patients with an obvious infection-related episode at onset, and correlated to expression levels of interferon response genes in plasmablasts. Collectively, these results imply that B cell responses in ME/CFS are directed against an infectious agents or priming antigens induced before disease onset.
The first one isn't exactly the same as the other two since they couldn't discriminate between IGHV3-23 and IGHV3-30, and the ME/CFS group seemed to have individuals with both very high and very low amounts of the combination of these gene segments:
Milivojevic et al said:Whilst 12 patients had extremely high levels (>100,000) of IGHV3-23/30, only 3 patients had extremely low levels (<25,000) of this protein.
I'm going to have to reread that one. I think I had misread before as it being IGHV3-23/30 on the BCR, but looks like it's actually antibodies in the first paper, with the following two being BCRs.
Here's the Ryback et al paper referencing the previous two studies:
BCR repertoire sequencing in ME/CFS and healthy controls (HCs) previously identified increased use of several Immunoglobulin Heavy Chain V (IGHV) gene segments in ME/CFS patients: IGHV-3-30 and IGHV3-30-3 gene usage was elevated in ME/CFS, particularly in patients who reported an infectious onset to their illness (19). The authors suggest this IGHV gene signature may represent a shared infection-elicited response among those ME/CFS patients.
This result putatively fits a signature of dysregulated IGHV3-30/IGHV3-23 antibody detected by plasma proteomic profiling (20).
With regard to COVID timing - I'm not sure about the Lipkin paper, though it was published near the start of the pandemic (2020), so the sample collection might have been before it. Sato et al says this:
Cohort 1 comprised patients recruited to NCNP hospital from October 2015 to December 2016. [...] To validate the results of BCR repertoire analysis, new patients with ME/CFS were recruited from NCNP hospital from January 2017 to November 2019, which comprised cohort 2
Ryback et al samples were from the CureME biobank, but I don't see dates of collection.
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