Human immunodeficiency virus long terminal repeat responds to T-cell activation signals.
Human immunodeficiency virus long terminal repeat responds to T-cell activation signals.
复制标题
人类免疫缺陷病毒长末端重复序列对 T 细胞激活信号作出反应。
DOI：
10.1073/pnas.84.19.6845
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发表时间：
1987
影响因子：
11.1
通讯作者：
B. Peterlin
中科院分区：
文献类型：
--
作者：
S. Tong;P. Luciw;B. Peterlin
人类免疫缺陷病毒（HIV）是艾滋病的病原体，感染并杀死携带CD 4抗原的淋巴细胞。在受感染的细胞中，许多细胞以及HIV编码的基因产物决定了病毒基因表达和HIV复制的水平。有效的HIV复制发生在活化的T细胞中。利用瞬时表达试验，我们表明，由HIV长末端重复序列（LTR）指导的基因表达增加响应T细胞激活信号。T细胞活化和HIV编码的反式激活因子（达特）的作用是倍增的。对HIV LTR中突变和缺失的分析揭示，响应T细胞活化信号的区域位于位置-105至-80。这些序列由两个同向重复序列组成，它们与猿猴病毒40基因组中的核心转录增强子元件同源。我们的研究表明，这些元素的功能作为艾滋病毒增强剂。通过直接作用于HIV LTR，T细胞活化可能在HIV基因表达和潜伏HIV的活化中起重要作用。
Human immunodeficiency virus (HIV), the causative agent of AIDS, infects and kills lymphoid cells bearing the CD4 antigen. In an infected cell, a number of cellular as well as HIV-encoded gene products determine the levels of viral gene expression and HIV replication. Efficient HIV-replication occurs in activated T cells. Utilizing transient expression assays, we show that gene expression directed by the HIV long terminal repeat (LTR) increases in response to T-cell activation signals. The effects of T-cell activation and of the HIV-encoded trans-activator (TAT) are multiplicative. Analysis of mutations and deletions in the HIV LTR reveals that the region responding to T-cell activation signals is located at positions -105 to -80. These sequences are composed of two direct repeats, which are homologous to the core transcriptional enhancer elements in the simian virus 40 genome. Our studies reveal that these elements function as the HIV enhancer. By acting directly on the HIV LTR, T-cell activation may play an important role in HIV gene expression and in the activation of latent HIV.