International Mammalian Genome Society

The 15th International Mouse Genome Conference (2001)


POSTER 11 - BONE MARROW CHIMERAS REVEAL A MAJOR, NON H-2, HEMATOPOIETIC CONTROL OF SUSCEPTIBILITY TO THEILER'S VIRUS PERSISTENT INFECTION

Mr Jean-François Bureau
Institut Pasteur
Unité des Virus Lents
28 rue du Dr. Roux
75724 Paris Cedex 15 France

Co-Authors:  Aubagnac S, Brahic M, and Bureau JF
Institution:   Unité des Virus Lents (URA CNRS 1930), Institut Pasteur 

Theiler's virus, a picornavirus, is responsible, in susceptible mice, for a persistent infection of the white matter of the spinal cord associated with chronic inflammation and primary demyelination. The viral load varies greatly among inbred mouse strains. For example, the SJL/J strain (H-2s) is persistently infected at a high level in contrast to the B10.S strain (H-2s) which clears the virus. The major part of this difference is due to two loci, Tmevp2 and Tmevp3, located on chromosome 10. Positional cloning for the Tmevp3 locus is well underway and we need to obtain functional informations concerning this locus. To determine whether the effect of the Tmevp3  locus is mediated by cells of hematopoietic or non hematopoietic origin, we created radiation bone marrow chimeras between the resistant B10.S and the susceptible SJL/J mice which bear the same H-2s haplotype. An SJL/J mouse congenic for the B10.S Tmevp3 region of the chromosome 10 was also studied. Resistant B10.S mice reconstituted with the bone marrow of the SJL/J mice become susceptible. Conversely, susceptible SJL/J mice reconstituted with the B10.S bone marrow become resistant. Therefore, the effect of these non H-2 loci on viral persistence is mainly mediated by hematopoietic cells. However, data obtained with the congenic mice complicate this simple model.


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