Researchers have demonstrated how B cells infected with the Epstein-Barr virus can contribute to a pathogenic, inflammatory phenotype that contributes to multiple sclerosis ; the group has also shown how these problematic B cells can be selectively targeted in a way that reduces the damaging autoimmune response of multiple sclerosis.
Though researchers know that EBV can contribute to the development of MS, the exact mechanisms by which it does so aren't completely understood. The Lieberman lab, in seeking to understand how EBV contributes to the development of MS, collaborated with Steven Jacobson, Ph.D., of the Neuroimmunology Branch at the National Institute of Neurological Disorders and Stroke, who contributed cell line samples from patients.
Diving further, Lieberman's group tested several antiviral compounds on all SLCL groups and found that one, TAF, reduced lytic EBV gene expression without killing the cells. TAF also significantly reduced the expression of inflammatory cytokines like IL-6 in the SLCLs from the patients with active MS.
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