Genetics: Chromosome 6 BTN2A2 and BTN3A3 (BTN2A1)

[ScoutB]

Awesome. Thanks for doing that @V.R.T.

 

[Chandelier]

https://www.virologie.uni-wuerzburg...oup-prof-dr-thomas-herrmann-senior-professor/ look in publications list of this guy

Welcome and thanks for joining us on the forum, @Claudia Schilling
Dr. Schilling, do you happen to know someone with connections to Professor Hermann who could help us to get the attention of his team?

 

[Chandelier]

Pretty random observation but Professor Hermann works at the University Würzburg and these guys have affiliations to the University Hospital Würzburg:

Thread 'Toleris Biotherapeutics'

Oct 14, 2026

Home | Toleris Biotherapeutics

toleris.com

From Twitter:

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Dr. rer. nat. Valentin Bruttel @VBruttel

Dear @weandmecfs, @MECFSResearch, @oeg_mecfs or any other ME/CFS-associated non-profit.

I am coordinating a research project at a university hospital to develop rapid, highly sensitive cell based diagnostics for functional GPCR autoantibodies and potentially to detect persistent viral infections by analyzing recirculating antigen-presenting cells (APCs).

Our immediate goal is to investigate the most likely cause of severe ME/CFS in a teenage girl...​

• Chandelier
• biotech germany mecfs
• Replies: 5
• Forum: ME/CFS research news

• 

 

[fst]

forestglip's post for another study gave me the idea to split the analysis by onset-type to find out whether a gene contributes by making individuals more prone to acute infection or by actually contributing to the ongoing disease process. Unfortunately, onset type is probably not available for the study in the post.

This is most likely old news for everyone but me, but DecodeME did just that. The odds ratio for BTN is almost identical between Infectious and Non-Infectious onset.

Does that imply that the role of BTN is likely not due to its role in acute infection (assuming non-infectious onset is actually Non-Infectious and not just a bit belated)?

DecodeME: BTN2A2 locus (chr6p22.2, lead variant 6:26239176:A:G) by onset type

GWAS	Cases	Controls	Effect allele freq.	OR (95% CI)	-log10 p
GWAS-Infection	9,738	259,909	0.261	1.086 (1.050–1.123)	5.77*
GWAS-No-Infection	5,841	259,909	0.261	1.083 (1.038–1.130)	3.68

*"No-Infection" includes participants who answered "Don't know" about infection at onset.

 

[forestglip]

Does that imply that the role of BTN is likely not due to its role in acute infection (assuming non-infectious onset is actually Non-Infectious and not just a bit belated)?

Good thing to check. I think that does provide some evidence that the BTN locus is not causing ME/CFS by making people more susceptible to symptomatic acute infections.

 

[Jonathan Edwards]

by making people more susceptible to symptomatic acute infections.

It is also probably a signpost away from immune responses to infections as being critical. Immune responses might still be involved in some cases - maybe invoking gamma delta T cells or macrophages - but maybe as optional pathway in to the central problem.

I think that James Cox's point that cerebellum may come up on gene expression studies simply because of the extraordinary density of synapses there compared to other sites. So we can probably forget Bergman cells.

 

[Kitty]

Does that imply that the role of BTN is likely not due to its role in acute infection (assuming non-infectious onset is actually Non-Infectious and not just a bit belated)?

Another point is that people who report non-infectious onset can only know whether or not they had symptoms of an infection. I didn't have any, but that doesn't guarantee there wasn't an immune response going on.

I might even have been tired or headachy, but it's not unusual enough to remember. Specially for women whose menstrual cycles make them feel tired and headachy every four weeks.