Eis-Hübinger A M, Schneweis K E
Institut für Medizinische Mikrobiologie und Immunologie, Universität Bonn.
Monatsschr Kinderheilkd. 1991 Jul;139(7):391-5.
The latent herpes simplex virus (HSV) infection is the source of multiple recurrent infections with this virus. Viral latency is the result of different specific and nonspecific defense mechanisms. Factors of the nonspecific defense system protect against the viral spread from the peripheral inoculation site via the lymphohaematogenous pathway. Therefore, viral spread is restricted to the neural route. Elimination of infection in the highly HLA class I-antigens expressing epithelial cells is caused by the cell-mediated immunity interrupting further virus invasion into the sensory and autonomous ganglia. In the bradytrophic neuronal cells, virus replication is moderate in comparison to epithelial cells. Here, the virus elimination and latency is mainly induced by the humoral immune response, probably because of the low level of expressed HLA-antigens. The relevance of the various immune mechanisms is demonstrated for some clinical situations, such as infection during pregnancy, in newborns and immunocompromised patients, exogenous reinfection and endogenous recurrence.
潜伏的单纯疱疹病毒(HSV)感染是该病毒多次复发感染的根源。病毒潜伏是不同特异性和非特异性防御机制的结果。非特异性防御系统的因素可防止病毒通过淋巴血行途径从外周接种部位扩散。因此,病毒传播仅限于神经途径。在高表达HLA-I类抗原的上皮细胞中,感染的消除是由细胞介导的免疫中断病毒进一步侵入感觉神经节和自主神经节所致。在生长缓慢的神经元细胞中,与上皮细胞相比,病毒复制较为适度。在这里,病毒的消除和潜伏主要由体液免疫反应诱导,这可能是由于HLA抗原表达水平较低。各种免疫机制的相关性在一些临床情况下得到了证实,如孕期感染、新生儿感染、免疫功能低下患者感染、外源性再感染和内源性复发。