Bureau J F, Montagutelli X, Bihl F, Lefebvre S, Guénet J L, Brahic M
Unité des Virus Lents, CNRS UA1157, Paris, France.
Nat Genet. 1993 Sep;5(1):87-91. doi: 10.1038/ng0993-87.
Inbred strains of mice differ greatly in their susceptibility to the demyelinating disease caused by Theiler's Murine Encephalomyelitis Virus. In this murine disease, which is an animal model for the study of multiple sclerosis, demyelination depends on the persistent infection of the central nervous system. Previous studies identified a locus in the H-2D region of the major histocompatibility complex which controls susceptibility to the persistent infection, and also showed that other loci are involved. In order to identify these loci, we screened the genome of a set of backcross animals with a combination of polymorphic microsatellites and restriction enzymes sites. We now show that viral persistence is also controlled by a locus close to Ifg on chromosome 10 and possibly by a locus near Mbp on chromosome 18.
近交系小鼠对由泰勒氏鼠脑脊髓炎病毒引起的脱髓鞘疾病的易感性差异很大。在这种作为多发性硬化症研究动物模型的鼠类疾病中，脱髓鞘取决于中枢神经系统的持续感染。先前的研究在主要组织相容性复合体的H-2D区域确定了一个控制对持续感染易感性的基因座，并且还表明其他基因座也参与其中。为了确定这些基因座，我们用多态性微卫星和限制性酶切位点的组合筛选了一组回交动物的基因组。我们现在表明，病毒持续性也受10号染色体上靠近Ifg的一个基因座控制，可能还受18号染色体上靠近Mbp的一个基因座控制。
