向性
发病机制
免疫学
疾病
病毒学
病毒
人类免疫缺陷病毒(HIV)
组织向性
医学
生物
病理
出处
期刊:Science
[American Association for the Advancement of Science]
日期:1993-05-28
卷期号:260 (5112): 1273-1279
被引量:672
标识
DOI:10.1126/science.8493571
摘要
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.
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