Rosenberg Z F, Fauci A S
National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.
Immunol Today. 1990 May;11(5):176-80. doi: 10.1016/0167-5699(90)90070-p.
In this paper Zeda Rosenberg and Anthony Fauci review the prevailing hypotheses on the mechanisms by which human immunodeficiency virus (HIV) progressively and relentlessly destroys immune function in infected individuals. Although HIV can directly kill CD4+ T cells in vitro, the protracted course of HIV infection in vivo suggests that other pathogenic mechanisms are also involved. As a member of the lentivirus family, HIV can remain latent within the genome of the infected cell. Activation of HIV expression from a latent or low-level state of replication is dependent, in part, on the state of activation of the host cell. As a result, activation of HIV-infected CD4+ T cells or monocyte/macrophages during normal immune responses may ultimately result in the activation of HIV expression and spread of the infection. Thus, HIV may have developed the ability to use normal immune processes to its own reproductive advantage.
在本文中，泽达·罗森伯格和安东尼·福奇回顾了关于人类免疫缺陷病毒（HIV）在受感染个体中逐步且无情地破坏免疫功能的机制的主流假说。尽管HIV在体外可直接杀死CD4+ T细胞，但HIV在体内的漫长病程表明还涉及其他致病机制。作为慢病毒家族的一员，HIV可潜伏在受感染细胞的基因组内。HIV从潜伏或低水平复制状态的表达激活部分取决于宿主细胞的激活状态。因此，在正常免疫反应期间HIV感染的CD4+ T细胞或单核细胞/巨噬细胞的激活最终可能导致HIV表达的激活和感染的传播。这样一来，HIV可能已发展出利用正常免疫过程来实现自身繁殖优势的能力。
