Zinkernagel R M, Hengartner H
Institute of Experimental Immunology, University of Zurich, Switzerland.
Immunol Today. 1994 Jun;15(6):262-8. doi: 10.1016/0167-5699(94)90005-1.
It has been much debated as to whether CD4+ T-cell depletion and the pathogenesis of AIDS is the result of direct cytolytic effects of human immunodeficiency virus (HIV), T-cell apoptosis by nonspecific activation, dysregulation of cytokine production, or autoimmunity. In this context, Rolf Zinkernagel and Hans Hengartner discuss data from model infections with non-cytopathic viruses. They suggest that HIV may cause immunosuppression, not by direct cytolytic effects, but rather by a conventional virus-specific cytotoxic T-cell-mediated immunopathology.
关于CD4 + T细胞耗竭与艾滋病发病机制是否是人类免疫缺陷病毒(HIV)的直接细胞溶解作用、非特异性激活导致的T细胞凋亡、细胞因子产生失调或自身免疫的结果,一直存在很多争论。在这种背景下,罗尔夫·津克纳格尔和汉斯·亨加特纳讨论了来自非细胞病变病毒模型感染的数据。他们认为,HIV可能不是通过直接细胞溶解作用,而是通过传统的病毒特异性细胞毒性T细胞介导的免疫病理学导致免疫抑制。