Robert S. Fujinami

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


Robert S. Fujinami completed his PhD from Northwestern University and postdoctoral studies from the Scripps Research Institute. He is a Professor in the Department of Pathology at the University of Utah. He was the first recipient of the Harry Weaver Award from the National Multiple Sclerosis Society and he is a Jacob Javits Neuroscience recipient from NINDS, NIH. He has published more than 200 articles and has been serving as member on various editorial boards and NIH review panels.


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.

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