Dal Canto M C, Rabinowitz S G, Johnson T C
J Neurol Sci. 1979 Jun;42(1):155-68. doi: 10.1016/0022-510x(79)90159-x.
Infection of mice with a temperature-sensitive (ts) mutant of Chandipura virus (CV) ts472 CV, induced a slower disease than the respective parental virus and white matter lesions characterized by perivascular mononuclear infiltrates accompanied by primary demyelination. The pattern of these lesions was very similar to that in EAE, a prototypic autoimmune disease and in Theiler's virus infection in which an immunopathologic mechanism of myelin injury is strongly suggested. Results obtained in nude mice supported the possible immunopathological nature of myelin injury in ts472 CV infection. No inflammatory response was elicited in either grey or white matter. However, whereas grey matter presented extensive necrosis, no alterations were present in white matter. Such data suggest that whereas grey matter lesions are produced by direct viral cytolytic activity, white matter pathology is probably dependent on the host immune response for its development. The finding of additional models of virus-induced demyelination with a possible immunopathologic mechanism of myelin injury is significant as it suggests that this type of virus-induced myelin degeneration is not restricted to a single virus like Theiler's, but it may represent a more general mechanism of virus-induced demyelination.
用钱迪普拉病毒（CV）ts472 CV的温度敏感（ts）突变体感染小鼠，所引发的疾病进程比相应的亲代病毒更缓慢，且会出现白质病变，其特征为血管周围单核细胞浸润并伴有原发性脱髓鞘。这些病变的模式与实验性自身免疫性脑脊髓炎（一种典型的自身免疫性疾病）以及泰勒氏病毒感染中的病变模式非常相似，强烈提示了髓鞘损伤的免疫病理机制。在裸鼠身上获得的结果支持了ts472 CV感染中髓鞘损伤可能具有免疫病理性质的观点。在灰质和白质中均未引发炎症反应。然而，但灰质出现广泛坏死，而白质未出现任何改变。这些数据表明，虽然灰质病变是由病毒直接的细胞溶解活性产生的，但白质病变的发展可能依赖于宿主的免疫反应。发现具有可能的髓鞘损伤免疫病理机制的病毒诱导脱髓鞘的其他模型具有重要意义，因为这表明这种类型的病毒诱导的髓鞘变性并不局限于像泰勒氏病毒这样的单一病毒，而是可能代表了病毒诱导脱髓鞘的一种更普遍机制。
