Zack J A, Arrigo S J, Weitsman S R, Go A S, Haislip A, Chen I S
Department of Microbiology and Immunology, UCLA School of Medicine.
Cell. 1990 Apr 20;61(2):213-22. doi: 10.1016/0092-8674(90)90802-l.
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.
HIV-1对人类T淋巴细胞的有效感染依赖于被感染细胞的增殖。未增殖的静止T细胞可被HIV-1感染,并使病毒处于非激活状态,直至随后受到促有丝分裂刺激。我们采用一种经过改良的聚合酶链反应方法,该方法兼具灵敏性和定量性,以证明HIV-1 DNA合成在被感染的静止T细胞中启动的水平与激活的T细胞相当。然而,与激活的T细胞不同,病毒基因组在静止细胞中并未完全逆转录。尽管这种病毒DNA结构能够以潜伏形式在静止细胞中持续存在,但它不稳定。我们讨论了这种HIV-1 DNA结构的不稳定性与HIV-1的“自我限制持续性感染”的关系,并提出这可能解释了艾滋病患者循环系统中被感染细胞比例较低的原因。