This Is MS Multiple Sclerosis Knowledge & Support Community

This post is about a clinical trial, but I post it here before it will yield the answer to the new MS model.

Some time ago, MS was considered an autoimmune disease of T-cells. These cells were present in lesions (CD4+ and CD8+) and researchers were putting the blame on them, trying to deplete them to control the disease.

Since anti-CD20 depletion success (Rituxan) scientist now know that B-cells are involved, and in fact, CD8+ T-cells are supposed to be fighting the EBV-infected B-cells. Therefore something to boost.

The new idea of intervention is to inject patients with CD8+ cytotoxic T-cells to kill EBV-infected B-cells. Something similar to Rituxan but without secondary effects.

The clinical trial is still not recruiting, but is worth to follow its course:

Trial to Assess the Safety and Feasibility of Adoptive Cell Therapy With Autologous EBV-specific Cytotoxic T Lymphocytes (CTL) in Patients With a First Clinical Episode Highly Suggestive of Multiple Sclerosis (MS and EBV-CTL)

https://clinicaltrials.gov/ct2/show/NCT ... lls&rank=2

More evidence about EBV involvement.

Antibodies to the Epstein-Barr virus proteins BFRF3 and BRRF2 cross-react with human proteins

http://www.jni-journal.com/article/S0165-5728(17%2930236-9/fulltext?cc=y=

Abstract

We hypothesize that the immune response to Epstein-Barr virus (EBV) drives the autoimmune damage in multiple sclerosis (MS). We investigated whether antibodies to two EBV proteins targeted by MS patients cross-react with self proteins.

Using affinity columns, immunoprecipitation, and mass spectrometry, we found that antibodies to the EBV protein BFRF3 cross-react with the cytoplasmic protein septin-9, and antibodies to BRRF2 also bind mitochondrial proteins. Using Western blots and ELISA, we demonstrated that MS patients were more likely to have high levels of antibodies to one or another of these self antigens.

Highlights

•Antibodies to the Epstein-Barr virus proteins BFRF3 and BRRF2 are increased in MS.
•Antibodies to BFRF3 also bind the cytoskeletal protein septin-9.
•Antibodies to BRRF2 also bind the mitochondrial protein DLST.
•Most people have autoantibodies to septin-9 and many have autoantibodies to DLST. MS patients are more likely than controls to have high levels of antibodies to one of these two self proteins.
•Septin-9 has not been reported as an autoantigen before. DLST is a known autoantigen associated with primary biliary cirrhosis.
•We propose these cross-reactive autoimmune responses driven by Epstein-Barr virus infection could contribute to the pathogenesis of MS.

Would another viral infection causes the EBV to re-activate,?
I read that lack of oxygen could cause EBV to re-activate. Couldn't poor blood circulation through the CNS cause the EBV to re-activate?
Regards, Vesta

vesta wrote:Would another viral infection causes the EBV to re-activate,?
I read that lack of oxygen could cause EBV to re-activate. Couldn't poor blood circulation through the CNS cause the EBV to re-activate?
Regards, Vesta

Who knows. Anyway I would put by bets on Vitamin D levels.