Transcellular activation of the human immunodeficiency virus type 1 long terminal repeat in T lymphocytes requires CD4-gp120 binding.
Transcellular activation of the human immunodeficiency virus type 1 long terminal repeat in T lymphocytes requires CD4-gp120 binding.
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T 淋巴细胞中人类免疫缺陷病毒 1 型长末端重复序列的跨细胞激活需要 CD4-gp120 结合。
DOI：
10.1128/jvi.66.7.4536-4539.1992
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发表时间：
1992
影响因子：
5.4
通讯作者：
Weinberger,OK
中科院分区：
文献类型：
--
作者：
Marcuzzi,A;Lowy,I;Weinberger,OK
表达人类免疫缺陷病毒1型（HIV-1）达特的细胞可以在共培养的T淋巴细胞中反式激活HIV-1长末端重复序列（LTR）。在这份报告中，我们描述了跨细胞激活Jurkat细胞中的LTR的分子要求。缺失突变体和阻断抗体的分析表明，除了达特表达外，还需要env表达才能发生跨细胞活化。结果表明，在共培养的细胞中的CD 4和gp 120的瞬时协会所需的TAT介导的跨细胞活化。然而，与HIV介导的融合和感染相反，CD 4-gp 120反式激活结合后的事件不需要gp 120中和结构域。这种相互作用对细胞功能的影响目前正在研究中。
Cells expressing human immunodeficiency virus type 1 (HIV-1) tat can transactivate the HIV-1 long terminal repeat (LTR) in cocultured T lymphocytes. In this report, we describe the molecular requirements for transcellular activation of the LTR in Jurkat cells. An analysis with deletion mutants and blocking antibodies demonstrated a requirement for env expression in addition to tat expression for transcellular activation to occur. The results suggest that the transient association of CD4 and gp120 in cocultured cells is required for tat-mediated transcellular activation. The events that follow CD4-gp120 binding in transactivation, however, do not require the gp120-neutralizing domain, in contrast to HIV-mediated fusion and infection. The consequences of this interaction on cellular function are currently under investigation.