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Not all the research points to EBV. HERVs could be also involved.

"Preclinical research demonstrated that pathogenic HERV-W protein negatively impacts myelin restoration by directly inhibiting oligodendrocyte precursor cells (OPC), and induces inflammation by microglia activation"

"The retroviral envelope protein, encoded by a pathogenic member of the HERV-W family (pHERV-W env) has been identified in brain lesions of patients with MS, particularly in active lesions, and in the pancreas of type 1 diabetes (T1D) patients"

Source

http://www.geneuro.com/data/news/geneur ... -ms-en.pdf

Answering to myself, it seems that the HERVs retroviruses activation could be due to EBV. Therefore, it seems that all the evidence about HERV-W also points indirectly to EBV.

http://www.nrronline.org/article.asp?is ... ulast=Guan

... HERV-W activity (measured by MSRV-type transcript expression in peripheral blood mononuclear cells, PBMC) was higher in patients with infectious mononucleosis, and in healthy controls with high anti-EBV antibodies (Mameli et al., 2013). These findings suggest that silent MSRV may be activated by environmental triggers, such as an EBV infection, to directly contribute to MS development (Kury et al., 2018). Future studies are required for a better understanding of the role of MSRV and its interaction with EBV in the MS pathogenesis.