Key result
Theiler's virus persistence in macrophages drives Th1-mediated myelin damage requiring specific capsid conformations.
Why the study?
The molecular mechanisms underlying TMEV persistence and the resulting immunopathologic demyelinating disease in mice remain to be fully elucidated.
Population
Mice infected with Theiler's murine encephalomyelitis virus
Comparison
Wild-type TMEV versus recombinant and mutant TMEV viruses
Design
Review of molecular pathogenesis studies
Authors
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Preclinical TMEV data implicate capsid conformation in myelin damage; leaves open translation to human demyelinating disease.
TMEV persistence in macrophages leads to immune-mediated myelin damage, which is dependent on specific viral capsid conformations.
Upton et al. (1997) conducted a review in Theiler's murine encephalomyelitis virus-induced demyelinating disease. Theiler's murine encephalomyelitis virus (TMEV) infection was evaluated. Theiler's murine encephalomyelitis virus persistence in macrophages leads to immunopathologic myelin damage mediated by Th1 lymphocytes, requiring specific capsid conformations for persistence.
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