Johnson R T
Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD.
Ann Neurol. 1994;36 Suppl(Suppl):S54-60. doi: 10.1002/ana.410360715.
Infectious agents have been postulated as causes of multiple sclerosis for over a century. The possible role of a virus or viruses is supported by data that (1) a childhood exposure is involved and "viral" infections may precipitate exacerbations of disease, (2) experimental infections in animals and natural infections in humans can cause diseases with long incubation periods, remitting and relapsing courses, and demyelination, and (3) patients with multiple sclerosis have abnormal immune responses to viruses. The pathogenesis of three human demyelinating diseases of known viral etiology is discussed. In progressive multifocal leukoencephalopathy, a papovavirus selectively infects oligodendrocytes and causes focal areas of demyelination. In postmeasles encephalomyelitis, the virus is lymphotrophic and disrupts immune regulation that can result in an autoimmune perivenular demyelinating illness without evidence of infection of the central nervous system. In human immunodeficiency virus-encephalopathy and myelopathy virus is present in macrophages and microglia and the myelin abnormalities apparently are caused by soluble factors such as viral proteins, cytokines, or neurotoxins. These findings may have implications on how, when, and where to seek viruses in multiple sclerosis.
一个多世纪以来，感染因子一直被假定为多发性硬化症的病因。一种或多种病毒的可能作用得到了以下数据的支持：（1）涉及儿童期暴露，“病毒”感染可能会促使疾病恶化；（2）动物实验性感染和人类自然感染可导致潜伏期长、缓解和复发病程以及脱髓鞘的疾病；（3）多发性硬化症患者对病毒有异常的免疫反应。本文讨论了三种已知病毒病因的人类脱髓鞘疾病的发病机制。在进行性多灶性白质脑病中，一种乳头多瘤空泡病毒选择性感染少突胶质细胞并导致局灶性脱髓鞘区域。在麻疹后脑脊髓炎中，病毒具有嗜淋巴细胞性并破坏免疫调节，这可能导致一种自身免疫性血管周围脱髓鞘疾病，而中枢神经系统没有感染迹象。在人类免疫缺陷病毒相关性脑病和脊髓病中，病毒存在于巨噬细胞和小胶质细胞中，髓鞘异常显然是由病毒蛋白、细胞因子或神经毒素等可溶性因子引起的。这些发现可能对在多发性硬化症中寻找病毒的方式、时间和地点具有启示意义。
