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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

Unité des Virus Lents, CNRS URA 1930, Institut Pasteur, 28 rue du Dr Roux, 75724 Paris Cedex 15, France¹

Author for correspondence: Michel Brahic. Fax +33 1 40 61 31 67. e-mail mbrahic{at}pasteur.fr

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^bgene, 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gene or a chimeric H-2D^b/K^b gene in which the exons encoding the peptide-binding groove of the H-2K^b gene have been replaced by those of the H-2D^bgene. Mice transgenic for either the H-2D^bgene 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^bgene and the H-2K^b gene are due to the nature of the peptides presented by these class I molecules.

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