Wege H, Watanabe R, Koga M, Ter Meulen V
Prog Brain Res. 1983;59:221-31. doi: 10.1016/s0079-6123(08)63867-4.
Disease processes of the central nervous system (CNS) accompanied by demyelination may be the result of a viral infection or the consequence of an immunopathological reaction directed against myelin. In acute viral infections, the infection of oligodendroglial cells, leading to cell destruction, may be the main mechanism for inducing this neuropathological lesion. In the case of a persistent virus infection in oligodendroglia cells, however, it is conceivable that functional impairment of oligodendroglia cells, or the induction of an immune reaction to the agent that may cross-react with brain antigens, could eventually cause demyelination. Therefore, pathogenic studies on subacute or chronic demyelinating encephalomyelitides in association with viral infections may provide information on the mechanisms involved in demyelination. In rats, depending on the biological property of the virus material used, the genetic background and immune response of the host, a subacute or late demyelinating encephalomyelitis can be induced, accompanied by primary demyelination. This provides a model for analysis of the virus and host factors interacting in the pathogenesis of these diseases.
伴有脱髓鞘的中枢神经系统(CNS)疾病过程可能是病毒感染的结果,或者是针对髓鞘的免疫病理反应的后果。在急性病毒感染中,少突胶质细胞的感染导致细胞破坏,可能是诱发这种神经病理病变的主要机制。然而,在少突胶质细胞持续病毒感染的情况下,可以想象少突胶质细胞的功能受损,或者对可能与脑抗原发生交叉反应的病原体诱导免疫反应,最终可能导致脱髓鞘。因此,对与病毒感染相关的亚急性或慢性脱髓鞘性脑脊髓炎的致病性研究可能会提供有关脱髓鞘机制的信息。在大鼠中,根据所使用病毒材料的生物学特性、宿主的遗传背景和免疫反应,可以诱发亚急性或迟发性脱髓鞘性脑脊髓炎,并伴有原发性脱髓鞘。这为分析在这些疾病发病机制中相互作用的病毒和宿主因素提供了一个模型。