Gammaherpesvirus latency accentuates EAE pathogenesis: Relevance to Epstein-Barr virus and multiple sclerosis

Epstein-barr virus (ebv) has been identified as a putative environmental trigger of multiple sclerosis (ms),yet ebv's role in ms remains elusive. we utilized murine gamma herpesvirus 68 (γhv-68),the murine homolog to ebv,to examine how infection by a virus like ebv could enhance cns autoimmunity. mice latently infected with γhv-68 developed more severe eae including heightened paralysis and mortality. similar to ms,γhv-68eae mice developed lesions composed of cd4 and cd8 t cells,macrophages and loss of myelin in the brain and spinal cord. further,t cells from the cns of γhv-68 eae mice were primarily th1,producing heightened levels of ifn-γ and t-bet accompanied by il-17 suppression,whereas a th17 response was observed in uninfected eae mice. clearly,γhv-68 latency polarizes the adaptive immune response,directs a heightened cns pathology following eae induction reminiscent of human ms and portrays a novel mechanism by which ebv likely influences ms and other autoimmune diseases. © 2012 casiraghi et al.