Two new reports about EBV

[frodo]

The interaction of Multiple Sclerosis risk loci with Epstein-Barr virus phenotypes implicates the virus in pathogenesis

https://www.nature.com/articles/s41598-019-55850-z

Conclusion

We believe this paper presents compelling new evidence from the interaction between MS risk loci and EBV DNA copy number that host genetic variation affects EBV infection.

The over-representation of host genes associated with the EBV associated autoimmune diseases MS and SLE among these DNA-QTLs further implicates EBV in their disease pathogenesis. These data open up new approaches to controlling EBV that may be of therapeutic value. Specific molecular interactions between the expression of EBV miRNAs BART4-3p and BART3-5p, the MS risk gene PVR, and other MS risk loci with EBV DNA copy number and gene expression suggest they are useful targets for controlling EBV in MS.

Our findings are consistent with an EBV susceptibility signature contributing to risk of developing MS and SLE. These data provide strong support for further investigations into targeting the implicated EBV genes and processes to treat MS and other EBV associated diseases such as SLE, and cancers.


Epstein–Barr Virus in Multiple Sclerosis: Theory and Emerging Immunotherapies

https://www.sciencedirect.com/science/a ... 1419302941

New treatments for multiple sclerosis (MS) focused on B cells have created an atmosphere of excitement in the MS community.

B cells are now known to play a major role in disease, demonstrated by the highly impactful effect of a B cell-depleting antibody on controlling MS. The idea that a virus may play a role in the development of MS has a long history and is supported mostly by studies demonstrating a link between B cell-tropic Epstein–Barr virus (EBV) and disease onset.

Efforts to develop antiviral strategies for treating MS are underway. Although gaps remain in our understanding of the etiology of MS, the role, if any, of viruses in propagating pathogenic immune responses deserves attention.