Melvold R W, Jokinen D M, Miller S D, Dal Canto M C, Lipton H L
Department of Microbiology-Immunology, Northwestern University Medical School, Chicago, Illinois 60611.
J Virol. 1990 Feb;64(2):686-90. doi: 10.1128/JVI.64.2.686-690.1990.
Theiler's virus-induced demyelinating disease results from a chronic infection in the white matter of the central nervous system and provides an excellent model for human multiple sclerosis. Like multiple sclerosis, there are genetic risk factors in disease development, including genes associated with the major histocompatibility complex and with those encoding the beta chain of the T-cell receptor. Comparisons of the susceptible DBA/2 and resistant C57BL/6 strains have indicated an important role for the H-2D locus and for a non-H-2 gene (not involving the beta chain of the T-cell receptor) in differential susceptibility. In the present report, analysis of recombinant-inbred strains (BXD) between the DBA/2 and C57BL/6 strains indicated that this non-H-2 locus is located at the centromeric end of chromosome 3 near (4 +/- 4 centimorgans) the carbonic anhydrase-2 (Car-2) enzyme locus.
泰勒氏病毒诱导的脱髓鞘疾病源于中枢神经系统白质的慢性感染,为人类多发性硬化症提供了一个极佳的模型。与多发性硬化症一样,疾病发展存在遗传风险因素,包括与主要组织相容性复合体相关的基因以及编码T细胞受体β链的基因。对易感的DBA/2和抗性的C57BL/6品系的比较表明,H-2D基因座和一个非H-2基因(不涉及T细胞受体β链)在差异易感性中起重要作用。在本报告中,对DBA/2和C57BL/6品系之间的重组近交系(BXD)分析表明,这个非H-2基因座位于3号染色体着丝粒末端靠近碳酸酐酶-2(Car-2)酶基因座处(4±4厘摩)。