Hypothesis Ineffective control of Epstein-Barr-virus-induced autoimmunity increases the risk for multiple sclerosis, 2023, Vietzen et al.

That would be "in print"
(if I understand correctly that you mean that the paper has been accepted but not yet published by Cell)

And what an interesting study!

 

I think the long term mono study could throw up potentially interesting correlations if it could be funded for intermittent followups over a long time.

 

Sounds interesting, thanks for sharing. Let’s see what the paper will really entail (scientific news reports are of course highly unreliable and very clickbaity).

I couldn’t find a google scholar account, but Thomas Berger has a ResearchGate account https://www.researchgate.net/profile/Thomas-Berger-19/research.

Whilst I can’t read the news article, this was the programme of the conference https://apps.congrex.com/ectrims2023/en-GB/pag. There are quite a few names even familar to me in the EBV-MS field (Alberto Ascherio, William Robinson), so I guess it has to be quite a big conference. Thomas Berger gave a very short talk titled “Ineffective Immune Control of Epstein-Barr Virus-Induced Autoreactive Responses is an Important Cause of Multiple Sclerosis” in the session “Late Breaking Abstracts”.

 

Merged thread

Ineffective control of Epstein-Barr-virus-induced autoimmunity increases the risk for multiple sclerosis
Hannes Vietzen; Sarah M. Berger; Laura M. Kühner; Philippe L. Furlano; Gabriel Bsteh; Thomas Berger; Paulus Rommer; Elisabeth Puchhammer-Stöckl

Multiple sclerosis (MS) is a demyelinating disease of the CNS. Epstein-Barr virus (EBV) contributes to the MS pathogenesis because high levels of EBV EBNA386–405-specific antibodies cross react with the CNS-derived GlialCAM370–389. However, it is unclear why only some individuals with such high autoreactive antibody titers develop MS.

Here, we show that autoreactive cells are eliminated by distinct immune responses, which are determined by genetic variations of the host, as well as of the infecting EBV and human cytomegalovirus (HCMV). We demonstrate that potent cytotoxic NKG2C+ and NKG2D+ natural killer (NK) cells and distinct EBV-specific T cell responses kill autoreactive GlialCAM370–389-specific cells.

Furthermore, immune evasion of these autoreactive cells was induced by EBV-variant-specific upregulation of the immunomodulatory HLA-E. These defined virus and host genetic pre-dispositions are associated with an up to 260-fold increased risk of MS.

Our findings thus allow the early identification of patients at risk for MS and suggest additional therapeutic options against MS.

Highlights

• Control of autoimmunity by NKG2C + NK cell responses is severely impaired in MS patients
• MS-patient-derived GlialCAM-specific cells evade control via inhibitory HLA-E/NKG2A axis
• MS patients are predominantly infected with EBV variants that highly upregulate HLA-E
• Specific cytotoxic T cell responses can control EBV-infected GlialCAM-specific B cells

Link | PDF (Cell)

 

I suspect this is wishful thinking. Not long ago the antigen in MS was supposed to be something else. I doubt it has anything to do with cross reactivity.