DA Virus Mutant H101 Can Alter T-cell Mediated CNS Pathogenesis Through Virus Induced Immunosuppression | 28582
Journal of Neurological Disorders
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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.
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.
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