Robert S. Fujinami
University of Utah School of Medicine, USA
Title: DA virus mutant H101 can alter t cell mediated cns pathogenesis through virus induced immunosuppression
Biography
Biography: Robert S. Fujinami
Abstract
Viruses have immunomodulatory properties for the purpose of evading clearance by the host. We are investigating how a few changes in the Theiler’s murine encephalomyelitis virus (TMEV) genome could provide a means to suppress T cell mediated central nervous system (CNS) disease. The mutant TMEV virus, H101, in its natural host (the mouse), causes immunomodulation when administered via a peripheral route (intraperitoneal – i.p.). In contrast, C57BL/6 mice infected with the wild-type DA strain of TMEV via the i.p. route develop an asymptomatic infection and clear the virus. C57BL/6 mice infected with the H101 mutant virus via the i.p. route become immunosuppressed through the depletion of T cells. Intracerebral infection of C57BL/6 mice with lymphocytic choreomeningitis virus (LCMV) leads to death around day 6 post infection due to an aggressive anti-viral CD8+ T cell response. Infection of mice with H101 prior to infection with LCMV results in a majority of mice surviving past day 7 post-LCMV-infection. Similarly, infection, with H101, of mice with relapsing-remitting experimental autoimmune encephalomyelitis results in elimination of the CD4+ T cell mediated disease exacerbations. This study provides experimental evidence that viruses can be used to treat T cell mediated CNS disease.