ter Meulen V, Liebert U G
Institut für Virologie und Immunologie, Universität Würzburg, BRD.
Intervirology. 1993;35(1-4):86-94. doi: 10.1159/000150298.
Recovery from viral infection is a result of very complex interactions between specific and nonspecific immune reactions and the infectious agent. A variety of immune mechanisms are undoubtedly important factors in this event and operate together in overcoming the infectious process. However, despite much available information about these viral defense mechanisms, it has proved remarkably difficult to assign a determinative role in vivo to any single antiviral immunological mechanism in recovery from a single viral disease, particularly since the immune response to the virus itself may frequently contribute to the pathology of the disease. Furthermore, if virus-induced immune responses are also directed against normal host components, this may set the stage for an autoimmune disease. In this context acute measles encephalomyelitis is of interest since in this disease autoimmune reactions against brain antigens have been observed and considered of pathogenetic importance. In this short review, virological and immunological findings of measles virus infections in a rat model in relation to autoimmune reactions will be presented and the mechanisms by which measles virus may alter host reactivity against self-antigens discussed.
从病毒感染中恢复是特异性和非特异性免疫反应与感染因子之间非常复杂的相互作用的结果。多种免疫机制无疑是这一过程中的重要因素,并共同作用以克服感染过程。然而,尽管有很多关于这些病毒防御机制的信息,但事实证明,要确定任何单一抗病毒免疫机制在从单一病毒性疾病中恢复过程中的体内决定性作用非常困难,特别是因为对病毒本身的免疫反应可能经常导致疾病的病理变化。此外,如果病毒诱导的免疫反应也针对正常宿主成分,这可能会引发自身免疫性疾病。在这种情况下,急性麻疹脑脊髓炎很值得关注,因为在这种疾病中已经观察到针对脑抗原的自身免疫反应,并认为其具有致病重要性。在这篇简短的综述中,将介绍麻疹病毒感染大鼠模型中与自身免疫反应相关的病毒学和免疫学发现,并讨论麻疹病毒可能改变宿主对自身抗原反应性的机制。