Bureau J F, Drescher K M, Pease L R, Vikoren T, Delcroix M, Zoecklein L, Brahic M, Rodriguez M
Unite des Virus Lents, Centre National de la Recherche Scientifique ERS 572, Institut Pasteur, Paris, France.
Genetics. 1998 Apr;148(4):1941-9. doi: 10.1093/genetics/148.4.1941.
Theiler's murine encephalomyelitis virus causes a chronic demyelinating disease in susceptible strains of mice that is similar to human multiple sclerosis. Several nonmajor histocompatibility complex-linked genes have been implicated as determinants of susceptibility or resistance to either demyelination or virus persistence. In this study, we used linkage analysis of major histocompatibility complex identical H-2d (DBA/2J x B10.D2) F2 intercross mice to identify loci associated with susceptibility to virus-induced demyelinating disease. In a 20-cM region on chromosome 14, we identified four markers, D14Mit54, D14Mit60, D14Mit61, and D14Mit90 that are significantly associated with demyelination. Because two peaks were identified, one near D14Mit54 and one near D14Mit90, it is possible that two loci in this region are involved in controlling demyelination.
泰勒氏鼠脑脊髓炎病毒可在易感品系小鼠中引发一种慢性脱髓鞘疾病，该疾病与人类多发性硬化症相似。几个非主要组织相容性复合体连锁基因已被认为是决定对脱髓鞘或病毒持续存在易感性或抗性的因素。在本研究中，我们利用主要组织相容性复合体相同的H-2d（DBA/2J×B10.D2）F2杂交小鼠进行连锁分析，以确定与病毒诱导的脱髓鞘疾病易感性相关的基因座。在14号染色体上一个20厘摩的区域，我们鉴定出四个与脱髓鞘显著相关的标记，即D14Mit54、D14Mit60、D14Mit61和D14Mit90。由于鉴定出两个峰值，一个靠近D14Mit54，另一个靠近D14Mit90，因此该区域可能有两个基因座参与控制脱髓鞘。
