Weiss R A
Chester Beatty Laboratories, Institute of Cancer Research, London, United Kingdom.
Science. 1993 May 28;260(5112):1273-9. doi: 10.1126/science.8493571.
Many questions have been posed about acquired immunodeficiency syndrome (AIDS) pathogenesis. Is human immunodeficiency virus (HIV) both necessary and sufficient to cause AIDS? Is AIDS essentially an autoimmune disease, triggering apoptosis, or is virus infection the cause of T helper lymphocyte depletion? What is the significance of HIV tropism and the role of macrophages and dendritic cells in AIDS? Is there viral latency and why is there usually a long period between infection and AIDS? Is HIV variation a crucial aspect of its pathogenesis and, if so, do virulent strains emerge? Although this article provides few definitive answers, it aims to focus commentary on salient points. Overall, it is increasingly evident that both the tropism and burden of HIV infection correlate closely with the manifestations of disease.
关于获得性免疫缺陷综合征（艾滋病）的发病机制，人们提出了许多问题。人类免疫缺陷病毒（HIV）是导致艾滋病的必要且充分条件吗？艾滋病本质上是一种自身免疫性疾病，引发细胞凋亡，还是病毒感染导致辅助性T淋巴细胞耗竭？HIV嗜性的意义以及巨噬细胞和树突状细胞在艾滋病中的作用是什么？是否存在病毒潜伏，以及为什么感染与艾滋病之间通常有很长的间隔期？HIV变异是其发病机制的关键方面吗？如果是，是否会出现毒力菌株？尽管本文几乎没有给出明确答案，但旨在聚焦于突出要点进行评论。总体而言，越来越明显的是，HIV感染的嗜性和负荷都与疾病表现密切相关。
