HIV-1 ENTRY INTO QUIESCENT PRIMARY LYMPHOCYTES - MOLECULAR ANALYSIS REVEALS A LABILE, LATENT VIRAL STRUCTURE
HIV-1 ENTRY INTO QUIESCENT PRIMARY LYMPHOCYTES - MOLECULAR ANALYSIS REVEALS A LABILE, LATENT VIRAL STRUCTURE
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DOI：
10.1016/0092-8674(90)90802-l
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发表时间：
1990-04-20
期刊：
影响因子：
64.5
通讯作者：
CHEN, ISY
中科院分区：
文献类型：
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作者：
ZACK, JA;ARRIGO, SJ;CHEN, ISY
HIV-1对人T淋巴细胞的生产性感染依赖于受感染细胞的增殖。非增殖性静止T细胞可以被HIV-1感染，并在随后的促有丝分裂刺激之前以非活性状态窝藏病毒。我们使用的聚合酶链反应方法，这是敏感和定量的修改，以证明HIV-1的DNA合成开始在感染的静止T细胞的水平与活化的T细胞。然而，与活化的T细胞不同，病毒基因组在静止细胞中不完全逆转录。虽然这种病毒DNA结构可以作为潜伏形式存在于静止细胞中，但它是不稳定的。我们讨论了这种HIV-1 DNA结构的不稳定性与HIV-1“自我限制的持续感染”的关系，并提出这可能解释了艾滋病患者循环中感染细胞的低百分比。
Productive infection of human T lymphocytes by HIV-1 is dependent upon proliferation of the infected cell. Nonproliferating quiescent T cells can be infected by HIV-1 and harbor the virus in an inactive state until subsequent mitogenic stimulation. We use a modification of the polymerase chain reaction method, which is both sensitive and quantitative, to demonstrate that HIV-1 DNA synthesis is initiated in infected quiescent T cells at levels comparable with those of activated T cells. However, unlike that of activated T cells, the viral genome is not completely reverse transcribed in quiescent cells. Although this viral DNA structure can persist in quiescent cells as a latent form, it is labile. We discuss the lability of this HIV-1 DNA structure in relation to a "self-restricting persistent infection" by HIV-1 and propose that this may explain the low percentage of infected cells in the circulation of AIDS patients.