Transcellular activation of the human immunodeficiency virus type 1 long terminal repeat in cocultured lymphocytes.
Transcellular activation of the human immunodeficiency virus type 1 long terminal repeat in cocultured lymphocytes.
复制标题
共培养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。
DOI：
10.1128/jvi.66.7.4228-4232.1992
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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;Weinberger,J;Weinberger,OK
艾滋病进展的一个无法解释的方面是，在CD 4 + T辅助细胞耗竭发生之前，免疫异常是可检测的（A.R. Gruters，F. G.特普斯特拉河De Jong，C.J.M.货车诺奇，R.A.W.货车利耶和F. Miedema，Eur. 20：1039-1044，1990; F. Miedema，A.J. Chantal-Petit，F.G. Terpstra，J.K.M.E. Schattenkerk，F. de Wolf，B.J.M. Al，M.鲁什，J.M.A. Lang，S.A. Danner，J. Goudsmit和P.T.A. Schellekens，J. Clin. Invest. 82：1908-1914，1988; G.M.希勒，D.C.伯恩斯坦，K. S.董超生维亚河南卡罗来纳州雷德菲尔德萨拉赫丁和R.C. 137：2514-2521，1986）。在这份报告中，我们描述了一种机制，通过这种机制，人类免疫缺陷病毒1型（HIV-1）感染的细胞可以影响邻近的HIV-1感染的T淋巴细胞和未感染的T细胞。我们已经研究了T细胞和巨噬细胞系的相互作用，通过使用共培养的淋巴细胞与HIV-1 DNA转染。我们使用的HIV-1构建体缺乏功能性pol基因，因此不会产生感染性病毒。共培养导致共培养的T细胞中HIV长末端重复序列的跨细胞活化。这种跨细胞活化在共培养的3小时内就很明显，HIV表达细胞与靶细胞的比例低至1：1，000，并且依赖于Tat反应元件。少量表达HIV的细胞可以在短时间内影响大量未感染的旁观者细胞，这表明了一种机制，即整体免疫功能障碍可以先于感染细胞的高患病率。
One of the unexplained aspects of the progression of AIDS is that immunological abnormalities are detectable before CD4+ T-helper cell depletion occurs (A.R. Gruters, F.G. Terpstra, R. De Jong, C.J.M. Van Noesel, R.A.W. Van Lier, and F. Miedema, Eur. J. Immunol. 20:1039-1044, 1990; F. Miedema, A.J. Chantal-Petit, F.G. Terpstra, J.K.M.E. Schattenkerk, F. de Wolf, B.J.M. Al, M. Roos, J.M.A. Lang, S.A. Danner, J. Goudsmit, and P.T.A. Schellekens, J. Clin. Invest. 82:1908-1914, 1988; G.M. Shearer, D.C. Bernstein, K.S. Tung, C.S. Via, R. Redfield, S.Z. Salahuddin, and R.C. Gallo, J. Immunol. 137:2514-2521, 1986). In this report, we describe a mechanism by which human immunodeficiency virus type 1 (HIV-1)-infected cells can influence neighboring HIV-1-infected T lymphocytes and uninfected T cells as well. We have examined the interaction of T-cell and macrophage cell lines that are transfected with HIV-1 DNA by using cocultured lymphocytes. The HIV-1 constructs we used lack a functional pol gene and therefore do not produce infectious virus. Cocultivation results in the transcellular activation of the HIV long terminal repeat in the cocultured T cells. This transcellular activation is evident in as little as 3 h of cocultivation, at ratios of HIV-expressing cells to target cells as low as 1:1,000, and is dependent on the Tat-responsive element. The demonstration that a small number of HIV-expressing cells can affect a large number of uninfected bystander cells in a short period of time suggests a mechanism by which global immune dysfunction can precede the high prevalence of infected cells.