THE RESERVOIR FOR HIV-1 IN HUMAN PERIPHERAL-BLOOD IS A T-CELL THAT MAINTAINS EXPRESSION OF CD4
THE RESERVOIR FOR HIV-1 IN HUMAN PERIPHERAL-BLOOD IS A T-CELL THAT MAINTAINS EXPRESSION OF CD4
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DOI：
10.1126/science.2665081
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发表时间：
1989-07-21
期刊：
影响因子：
56.9
通讯作者：
FAUCI, AS
中科院分区：
文献类型：
--
作者：
SCHNITTMAN, SM;PSALLIDOPOULOS, MC;FAUCI, AS
人类免疫缺陷病毒1型（HIV-1）选择性感染表达CD4分子的细胞，导致获得性免疫缺陷综合征（AIDS）患者CD4+ T淋巴细胞功能出现大量定量和定性缺陷。然而，在任何给定时间，HIV-1感染者的外周血中只有极少数细胞表达病毒。先前的研究表明，HIV-1在体外感染CD4+ T细胞会导致CD4表达下调，从而在感染细胞表面不再检测到CD4蛋白。在本研究中，从艾滋病患者获得了高纯度的外周血单核细胞亚群（PBMCs），并通过荧光自动细胞分选纯化。采用病毒分离的方法进行检测，包括极限稀释分析、原位杂交、免疫荧光和基因扩增。在pbmc中，HIV-1在体内主要在T细胞亚群中表达，与体外观察相反，T细胞亚群继续表达CD4。这些表达hiv -1的细胞的前体频率约为1/1000 CD4+ T细胞。在所研究的所有HIV-1感染者中，CD4+ T细胞群含有HIV-1 DNA，在艾滋病患者中的频率至少为1/100细胞。这种高水平的感染可能是艾滋病患者CD4+ T细胞数量和功能进行性下降的主要原因。
Human immunodeficiency virus type 1 (HIV-1) selectively infects cells expressing the CD4 molecule, resulting in substantial quantitative and qualitative defects in CD4+ T lymphocyte function in patients with acquired immunodeficiency syndrome (AIDS). However, only a very small number of cells in the peripheral blood of HIV-1 infected individuals are expressing virus at any given time. Previous studies have demonstrated that in vitro infection of CD4+ T cells with HIV-1 results in downregulation of CD4 expression such that CD4 protein is no longer detectable on the surface of the infected cells. In the present study, highly purified subpopulations of peripheral blood mononuclear cells (PBMCs) from AIDS patients were obtained and purified by fluorescence-automated cell sorting. They were examined with the methodologies of virus isolation by limiting dilution analysis, in situ hybridization, immunofluorescence, and gene amplification. Within PBMCs, HIV-1 was expressed in vivo predominantly in the T cell subpopulation which, in contrast to the in vitro observations, continued to express CD4. The precursor frequency of these HIV-1-expressing cells was about 1/1000 CD4+ T cells. The CD4+ T cell population contained HIV-1 DNA in all HIV-1-infected individuals studied and the frequency in AIDS patients was at least 1/100 cells. This high level of infection may be the primary cause for the progressive decline in number and function of CD4+ T cells in patients with AIDS.