Seay A R, Wolinsky J S
Ann Neurol. 1982 Oct;12(4):380-9. doi: 10.1002/ana.410120411.
Ross River virus (strain T48) infection in mice causes an encephalomyelitis characterized by focal, primary demyelination in the cerebellum, brain stem, and spinal cord. Maximal serum and brain content of virus occurs on days 2 and 4, respectively. Virus is not detectable in serum after day 3 or in brain after day 9. Histopathological lesions are present by day 2 and consist of perivascular macrophage and polymorphonuclear leukocyte infiltration, focal necrosis in the internal granule cell layer, and myelin disruption. Mononuclear cell infiltrates are present by day 5. Foci of demyelination in the presence of preserved axons become more widespread by day 8, and early partial remyelination occurs by day 13. Immunosuppression reduces the mononuclear cell infiltration but does not alter the demyelination . Although the mechanism of Ross River virus-induced demyelination is not known, these findings suggest that it is not immune mediated.
罗斯河病毒（T48株）感染小鼠会引发一种脑脊髓炎，其特征为小脑、脑干和脊髓出现局灶性原发性脱髓鞘。病毒的最高血清含量和脑内含量分别出现在第2天和第4天。第3天后血清中检测不到病毒，第9天后脑内检测不到病毒。组织病理学损伤在第2天出现，包括血管周围巨噬细胞和多形核白细胞浸润、内颗粒细胞层的局灶性坏死以及髓鞘破坏。第5天出现单核细胞浸润。在轴突保留的情况下，脱髓鞘病灶在第8天变得更加广泛，第13天出现早期部分髓鞘再生。免疫抑制可减少单核细胞浸润，但不会改变脱髓鞘现象。尽管罗斯河病毒诱导脱髓鞘的机制尚不清楚，但这些发现表明其并非由免疫介导。
