Howcroft T K, Strebel K, Martin M A, Singer D S
Experimental Immunology Branch, National Cancer Institute, NIH, Bethesda, MD 20892.
Science. 1993 May 28;260(5112):1320-2. doi: 10.1126/science.8493575.
Major histocompatibility complex (MHC) class I molecules are the major receptors for viral peptides and serve as targets for specific cytotoxic T lymphocytes. Human immunodeficiency virus-type 1 (HIV-1) specifically decreased activity of an MHC class I gene promoter up to 12-fold. Repression was effected by the HIV-1 Tat protein derived from a spliced viral transcript (two-exon Tat). These studies define an activity for two-exon Tat distinct from that of one-exon Tat and suggest a mechanism whereby HIV-1-infected cells might be able to avoid immune surveillance, allowing the virus to persist in the infected host.
主要组织相容性复合体（MHC）I类分子是病毒肽的主要受体，也是特异性细胞毒性T淋巴细胞的靶标。人类免疫缺陷病毒1型（HIV-1）可使MHC I类基因启动子的活性特异性降低达12倍。这种抑制作用是由源自剪接病毒转录本（双外显子Tat）的HIV-1 Tat蛋白介导的。这些研究确定了双外显子Tat与单外显子Tat不同的活性，并提示了一种机制，通过该机制HIV-1感染的细胞可能能够逃避免疫监视，从而使病毒在受感染宿主中持续存在。
