Roos R P, Wollmann R
Ann Neurol. 1984 May;15(5):494-9. doi: 10.1002/ana.410150516.
DA strain of Theiler's murine encephalomyelitis virus produces a chronic, progressive demyelinating disease in mice that resembles multiple sclerosis. An immunopathological mechanism for demyelination has been postulated, because there is a brisk immune response with low virus titers at the time of demyelination and because immunosuppression lessens the degree of demyelination. We inoculated Nude mice with DA virus to clarify the role of immune-mediated demyelination. Animals became paralyzed 3 weeks to 2 months after inoculation, usually dying within a week of appearance of signs. Demyelinated foci were present in the spinal cords, with evidence of degenerating myelin around intact axons as well as completely demyelinated, naked axons. Occasional macrophages were present, but none was seen actively stripping intact myelin lamellae. These results suggest that DA virus lytic infection, without a contribution from the T lymphocyte immune system, is sufficient to produce demyelination. It is likely that DA virus demyelination has varying mechanisms that may be active at different times.
泰勒氏小鼠脑脊髓炎病毒的DA毒株可在小鼠中引发一种类似于多发性硬化症的慢性进行性脱髓鞘疾病。已经提出了一种脱髓鞘的免疫病理机制,因为在脱髓鞘时存在活跃的免疫反应且病毒滴度较低,并且免疫抑制会减轻脱髓鞘的程度。我们给裸鼠接种DA病毒以阐明免疫介导的脱髓鞘作用。接种后3周 至2个月动物出现麻痹,通常在出现症状后一周内死亡。脊髓中存在脱髓鞘病灶,有证据表明完整轴突周围的髓鞘正在退化,以及完全脱髓鞘的裸露轴突。偶尔可见巨噬细胞,但未观察到有巨噬细胞积极剥脱完整的髓鞘板层。这些结果表明,DA病毒的溶细胞性感染,在没有T淋巴细胞免疫系统参与的情况下,足以导致脱髓鞘。DA病毒引起的脱髓鞘可能有不同的机制,这些机制可能在不同时间起作用。