Abstract
Theiler's murine encephalomyelitis virus is a picornavirus which induces chronic immune-mediated central nervous system demyelination and virus persistence in susceptible strains of mice. Using murine strains with congeneic recombinant haplotypes, the H-2D region within the class I major histocompatibility complex has been shown to be important in determining susceptibility/resistance to chronic Theiler's murine encephalomyelitis virus infection. We examined the role of H-2D in demyelinating disease with the use of transgenic D8 mice (H-2Dd, resistant haplotype) crossed to susceptible B10.Q (H-2q) and B10.S (H-2s) mice. Expression of the H-2Dd transgene dramatically suppressed demyelination and reduced the number of virus-antigen positive cells in the spinal cord 45 days following infection. More complete protection was observed in transgenic B10.Q (D8+) mice than in transgenic B10.S (D8+) mice. These experiments support the hypothesis that the immunologic basis of resistance by H-2D is determined by effective antigen presentation which prevents virus persistence and subsequent demyelination.
Original language | English (US) |
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Pages (from-to) | 111-117 |
Number of pages | 7 |
Journal | Journal of neurovirology |
Volume | 1 |
Issue number | 1 |
DOIs | |
State | Published - Mar 1995 |
ASJC Scopus subject areas
- Neurology
- Clinical Neurology
- Cellular and Molecular Neuroscience
- Virology