Roles of the H-2D b and H-K b genes in resistance to persistent Theiler's murine encephalomyelitis virus infection of the central nervous system
Abstract
Theiler's murine encephalomyelitis virus, a member of the Picornaviridae family, persists in the spinal cord of susceptible strains of mice. Resistant strains of mice, such as the H-2 b strain, clear the virus infection after an acute encephalomyelitis. The H-2D locus, but not the H-2K locus, has a major effect on this resistance, although both loci code for MHC class I molecules with similar general properties. For the present work, we rendered susceptible H-2 q FVB/N mice transgenic for either the H-2D b gene, the H-2K b gene or a chimeric H-2D b /K b gene in which the exons encoding the peptide-binding groove of the H-2K b gene have been replaced by those of the H-2D b gene. Mice transgenic for either the H-2D b gene or the chimeric H-2D b /K b gene were significantly more resistant to persistent virus infection than mice transgenic for the H-2K b gene, suggesting that the difference in the effects of the H-2D b gene and the H-2K b gene are due to the nature of the peptides presented by these class I molecules.