Roles of the H-2D(b) and H-K-b genes in resistance to persistent Theiler'smurine encephalomyelitis virus infection of the central nervous system

Theiler's murine encephalomyelitis virus, a member of the Picornaviridae fa mily, 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 afte r 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 m olecules 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gene or a chimeric H-2D(b)/K-b gene in which the exons encoding the peptide-binding groove of the H-2K(b) gene have been replaced by those of the H-2D(b) gene.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 chimer ic H-2D(b)/K-b gene were significantly more resistant to persistent virus i nfection than mice transgenic for the H-2Kb gene, suggesting that the diffe rence in the effects of the H-2D(b) gene and the H-2K(b) gene are due to th e nature of the peptides presented by these class I molecules.