Pathogenesis of the slow disease of the central nervous system associated with WM 1504 E virus. I. Relationship of strain susceptibility and replication to disease.
Pathogenesis of the slow disease of the central nervous system associated with WM 1504 E virus. I. Relationship of strain susceptibility and replication to disease.
复制标题
与 WM 1504 E 病毒相关的中枢神经系统慢性疾病的发病机制。
作者：
M. Oldstone;P. Lampert;S. Lee;F. Dixon
近交系小鼠对WM1504E病毒引起的慢性神经系统疾病的易感性有很大差异。尽管所有接种病毒的菌株都显示出病毒复制的证据，但这些注定要发展成慢性病的菌株在其血清和组织中，特别是在中枢神经系统中，病毒抗原的滴度始终高于耐药菌株。对感病品系C57BR/CDJ与抗性品系C57BL/6J杂交的研究表明，抗性是显性的，而不是性连锁的。损伤的主要区域包括脊髓前角的神经元、小脑齿状核和脑干的其他核团。少突胶质细胞参与相关的原发性脱髓鞘也被注意到。组织损伤伴有强烈的胶质细胞增厚，但未见白细胞浸润。免疫病理研究和副生物实验表明，组织损伤可能是由于主要的直接病毒作用。此外，胸腺不足的裸鼠患上了这种慢性神经疾病。
Inbred mouse strains vary considerably in their susceptibility to the chronic neurologic disease caused by WM 1504 E virus. Although all strains inoculated with the virus showed evidence of viral replication, those strains destined to develop chronic disease showed consistently higher titers of viral antigen in their sera and also in their tissues, particularly in the central nervous system, than did resistant strains. Studies of hybrids made by mating susceptible C57BR/cdJ and resistant C57BL/6J strains indicated that resistance is dominant and not sex linked. The major areas of injury included neurons in the anterior horn of the spinal cord, the dentate nucleus of the cerebellum, and other nuclei in the brain stem. Involvement of oligodendrocytes with associated primary demyelination was also noted. Tissue damage accompanied intense gliosis but was without leukocyte infiltration. Immunopathologic studies and parabiotic experiments suggested that tissue injury was likely due to primary direct viral effects. Further, thymus-insufficient nude mice developed this chronic neurologic disease.