Watanabe R, Wege H, ter Meulen V
Nature. 1983;305(5930):150-3. doi: 10.1038/305150a0.
Viruses have been found to induce inflammatory demyelinating lesions in central nervous system (CNS) tissue of both animal and man, either by natural infections or after vaccination. At least two different pathogenic mechanisms have been proposed for these changes, a cytopathic viral infection of oligodendroglia cells with subsequent cell death, and a host immune reaction against virus and brain antigens. We now report the occurrence of cell-mediated immune reactions against basic myelin proteins in the course of coronavirus infections in Lewis rats. Infection of rats with the murine coronavirus JHM leads to demyelinating encephalomyelitis developing several weeks to months postinfection. Lymphocytes from these diseased Lewis rats can be restimulated with basic myelin protein (BMP) and adoptive transfer of these cells leads to lesions resembling those of experimental allergic encephalomyelitis (EAE) in recipients, which can be accompanied by a mild clinical disease. This model demonstrates that a virus infection in CNS tissue is capable of initiating an autoimmune response which may be of pathogenic importance.
已发现病毒可通过自然感染或接种疫苗后，在动物和人类的中枢神经系统（CNS）组织中诱发炎性脱髓鞘病变。针对这些变化至少提出了两种不同的致病机制，即少突胶质细胞的细胞病变性病毒感染及随后的细胞死亡，以及宿主针对病毒和脑抗原的免疫反应。我们现在报告在Lewis大鼠冠状病毒感染过程中发生了针对碱性髓鞘蛋白的细胞介导免疫反应。用鼠冠状病毒JHM感染大鼠会导致感染后数周或数月出现脱髓鞘性脑脊髓炎。这些患病Lewis大鼠的淋巴细胞可用碱性髓鞘蛋白（BMP）再次刺激，将这些细胞进行过继性转移会使受体出现类似于实验性变应性脑脊髓炎（EAE）的病变，并可能伴有轻度临床疾病。该模型表明，中枢神经系统组织中的病毒感染能够引发自身免疫反应，这可能具有致病重要性。
