Watanabe R, Wege H, ter Meulen V
Institut für Virologie und Immunbiologie, Universität Würzburg.
Lab Invest. 1987 Oct;57(4):375-84.
Lewis and Brown Norway rats were infected at different ages with the neurotropic murine coronavirus strain, JHM and the resultant central nervous system diseases were studied. Suckling rats of both strains came down with a fatal, acute encephalomyelitis. Weanling Lewis rats developed a subacute demyelinating encephalomyelitis which neuropathologically revealed changes of an immunopathologic reaction. In contrast, Brown Norway rats developed a clinically silent subacute demyelinating encephalomyelitis with a persistent JHM virus infection which was less severe and quite different from the subacute demyelinating encephalomyelitis in Lewis rats with respect to size, distribution, and localization of the demyelinating plaques as well as the type of infiltrating cells. In addition, infected Lewis rats showed a pronounced lymphocyte proliferation to myelin basic protein and JHM virus whereas lymphocytes from infected Brown Norway rats did not react to these two antigens. These observations demonstrate the pathogenetic importance of host factors in the development of virus-induced demyelination.
将不同年龄段的Lewis大鼠和棕色挪威大鼠用嗜神经性鼠冠状病毒JHM株进行感染，并对由此产生的中枢神经系统疾病进行研究。两种品系的乳鼠均患上了致命的急性脑脊髓炎。断奶后的Lewis大鼠发展为亚急性脱髓鞘性脑脊髓炎，神经病理学显示有免疫病理反应的变化。相比之下，棕色挪威大鼠发展为临床上无症状的亚急性脱髓鞘性脑脊髓炎，伴有持续的JHM病毒感染，其病情较轻，在脱髓鞘斑块的大小、分布和定位以及浸润细胞类型方面与Lewis大鼠的亚急性脱髓鞘性脑脊髓炎有很大不同。此外，感染的Lewis大鼠对髓鞘碱性蛋白和JHM病毒表现出明显的淋巴细胞增殖，而感染的棕色挪威大鼠的淋巴细胞对这两种抗原无反应。这些观察结果证明了宿主因素在病毒诱导的脱髓鞘发展中的发病机制重要性。
