Robert S. Fujinami
Professor of Pathology
Neurobiology of Disease
Brain and Behavior
e-mail: robert.fujinami@hsc.utah.edu
B.A. 1972, University of Utah; Ph.D. 1977, Northwestern University
RESEARCH:
Neuroimmunology/Neurovirology - Understanding immune and viral contributions to the pathogenesis of multiple sclerosis and epilepsy
Virus infection leading to central nervous system (CNS) demyelination.
Theiler's virus causes an encephalomyelitis in mice and this infection mimics multiple
sclerosis (MS) in humans. The virus spreads through the CNS and infects white matter
particularly the oligodendrocytes and astrocytes. This project involves understanding
the virologic and immunologic participation in this CNS demyelinating disease.
How virus infection modulates immune responses leading to autoimmune disease.
Genetically altered viruses encoding myelin proteins can either protect against or
enhance an autoimmune disease known as experimental allergic encephalomyelitis (EAE).
This is a model for the human disease, MS. These data were generated using viruses
encoding myelin basic protein, and myelin proteolipid protein. Other viral constructs
coding for other CNS proteins need to be characterized. This project involves definition
of how these viral constructs can modulate immune responses and whether infection
leads to autoimmune disease.
Virus Infection and Epilepsy.
We have created a new infectious agent model for temporal lobe epilepsy. In our previous
studies, SJL/J mice infected with Theiler's murine encephalomyelitis virus (TMEV)
develop a persistent viral infection with an inflammatory demyelinating pathology
in the CNS. In recent studies, C57BL/6 mice infected with TMEV develop acute seizures
that resolve and later have spontaneous seizures. TMEV in C57BL/6 mice targets the
hippocampus. The ensuing acute innate inflammatory response contributes to the acute
seizures. We are investigating the contributions of the innate immune response to
the acquisition of seizures.