| First Author | Azoulay-Cayla A | Year | 2001 |
| Journal | J Gen Virol | Volume | 82 |
| Issue | Pt 5 | Pages | 1043-1047 |
| PubMed ID | 11297678 | Mgi Jnum | J:292871 |
| Mgi Id | MGI:6435874 | Doi | 10.1099/0022-1317-82-5-1043 |
| Citation | Azoulay-Cayla A, et al. (2001) 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. J Gen Virol 82(Pt 5):1043-1047 |
| abstractText | 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gene or a chimeric H-2D(b)/K(b) gene in which the exons encoding the peptide-binding groove of the H-2K(b) gene have been replaced by those of the H-2D(b)gene.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. |
