Zinkernagel R M
University of Zurich, Institute of Experimental Immunology, Switzerland.
Adv Exp Med Biol. 1995;374:165-71. doi: 10.1007/978-1-4615-1995-9_14.
HIV is basically a non- or poorly cytocidal virus. Therefore, HIV infections in humans represent an apparent perversity in the balance between the host immune system and infectious agent: This noncytopathic virus infects macrophages, antigen presenting cells, helper T cells and other host cells which are then destroyed by the CD8+ T cell immune response. Thus, HIV infects some of the key cells involved in immune reactions and therefore induces the immune system to destroy itself and thereby enables the virus to persist. Accordingly, immunosuppression is not a cause of HIV cytopathogenicity but a consequence of conventional T cell mediated immunopathology that destroys macrophages antigen presenting cells, T helper cells and facilitates infection by trivial intracellular parasites which eventually cause fatal disease. This immunopathological view of AIDS is testable and, if correct, impinges on rationales for AIDS prevention and treatment.
HIV本质上是一种非杀细胞性或弱杀细胞性病毒。因此,人类感染HIV代表了宿主免疫系统与感染因子之间平衡的一种明显反常情况:这种非细胞病变性病毒感染巨噬细胞、抗原呈递细胞、辅助性T细胞及其他宿主细胞,随后这些细胞被CD8 + T细胞免疫反应所破坏。因此,HIV感染了一些参与免疫反应的关键细胞,从而诱导免疫系统自我毁灭,进而使病毒得以持续存在。相应地,免疫抑制不是HIV细胞致病性的原因,而是传统T细胞介导的免疫病理学的结果,这种免疫病理学破坏巨噬细胞、抗原呈递细胞、辅助性T细胞,并促进微不足道的细胞内寄生虫感染,最终导致致命疾病。这种关于艾滋病的免疫病理学观点是可以检验的,如果正确,将影响艾滋病预防和治疗的基本原理。