Houtman J J, Fleming J O
Department of Medical Microbiology, University of Wisconsin, Madison 53706, USA.
J Neurovirol. 1996 Dec;2(6):361-76. doi: 10.3109/13550289609146902.
Infection of rodents with neurotropic mouse hepatitis virus (MHV) may result in lethal encephalitis or paralytic demyelinating disease resembling the human disease multiple sclerosis. The outcome of MHV infection is dependent on a number of variables, including the passage history of the viral isolate, dose and route of inoculation, and the age and immune status of the host. Alterations in surface glycoproteins, especially the spike protein, can profoundly influence pathogenesis. Innate resistance to MHV infection may be related to the expression of cellular receptors or to immunological factors. The immune system plays a major role in MHV pathogenesis, affecting encephalitis, viral clearance, and demyelination. Antiviral antibodies, CD4+ T lymphocytes, or CD8+ T lymphocytes may protect infected animals from lethal encephalitis, but both CD4+ and CD8+ T lymphocytes are required for effective viral clearance. Demyelination in MHV-infected animals has been attributed to the cytolytic effects of viral infection on myelin-producing oligodendrocytes, but more recent evidence supports an immunopathological mechanism for demyelination. Immunopathological models for demyelination include autoimmunity, direct immune cytotoxicity, and indirect 'bystander' damage. Although evidence exists supporting all of these models, the authors favor the bystander demyelination model. Much remains to be revealed about the processes leading to demyelination in MHV-infected mice, and information gained from these investigations may aid in the study of demyelinating disease in humans.
啮齿动物感染嗜神经小鼠肝炎病毒（MHV）可能导致致命性脑炎或类似人类疾病多发性硬化症的麻痹性脱髓鞘疾病。MHV感染的结果取决于多个变量，包括病毒分离株的传代历史、接种剂量和途径，以及宿主的年龄和免疫状态。表面糖蛋白的改变，尤其是刺突蛋白，可深刻影响发病机制。对MHV感染的先天抵抗力可能与细胞受体的表达或免疫因素有关。免疫系统在MHV发病机制中起主要作用，影响脑炎、病毒清除和脱髓鞘。抗病毒抗体、CD4 + T淋巴细胞或CD8 + T淋巴细胞可能保护感染动物免受致命性脑炎，但有效清除病毒需要CD4 +和CD8 + T淋巴细胞。MHV感染动物的脱髓鞘归因于病毒感染对产生髓磷脂的少突胶质细胞的细胞溶解作用，但最近的证据支持脱髓鞘的免疫病理机制。脱髓鞘的免疫病理模型包括自身免疫、直接免疫细胞毒性和间接“旁观者”损伤。虽然有证据支持所有这些模型，但作者倾向于旁观者脱髓鞘模型。关于MHV感染小鼠中导致脱髓鞘的过程仍有许多有待揭示，从这些研究中获得的信息可能有助于人类脱髓鞘疾病的研究。
