Monokine regulation of human immunodeficiency virus-1 expression in a chronically infected human T cell clone.
Monokine regulation of human immunodeficiency virus-1 expression in a chronically infected human T cell clone.
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DOI：
10.4049/jimmunol.142.2.431
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发表时间：
1989-01
影响因子：
4.4
通讯作者：
K. Clouse;D. Powell;I. Washington;Guido Poli;K. Strebel;W. Farrar;P. Barstad;J. Kovacs;A. Fauci;T. Folks
中科院分区：
文献类型：
--
作者：
K. Clouse;D. Powell;I. Washington;Guido Poli;K. Strebel;W. Farrar;P. Barstad;J. Kovacs;A. Fauci;T. Folks
从感染人类免疫缺陷病毒1型（HIV - 1）的T细胞中获得的一个T细胞克隆（ACH - 2），在受到一种富含单核因子的上清液刺激时会产生HIV - 1，这种上清液是通过用细菌脂多糖（LPS）培养人单核细胞/巨噬细胞而制备的（LPS - MO SN）。单核因子对ACH - 2细胞的诱导导致病毒产量增加，这反映在逆转录酶活性的提高以及所有主要病毒蛋白的合成上。通过间接免疫荧光对细胞进行检测发现，10% - 15%的未诱导细胞组成性地表达HIV蛋白，而在LPS - MO SN刺激下，100%的细胞显示出阳性免疫荧光。LPS - MO SN对病毒的这种诱导使得感染性病毒产量比未诱导的ACH - 2细胞增加了约100倍。单独的LPS不能诱导HIV - 1表达，而LPS - MO SN导致了最大程度的病毒表达。细胞分离研究证实诱导因子来源于带有成熟单核细胞/巨噬细胞标志物Leu M3的细胞。对LPS - MO SN进行的生化分级分离表明，一种或多种表观分子量约为45 kDa的因子参与了这种诱导。用对人肿瘤坏死因子 - α具有特异性的免疫亲和凝胶吸收LPS - MO SN，结果显示完全去除了对ACH - 2细胞系的HIV诱导活性。
A T cell clone (ACH-2) derived from T cells infected with HIV-1 was found to produce HIV-1 in response to stimulation with a monokine-enriched supernatant prepared by culturing human monocyte/macrophages with bacterial LPS (LPS-MO SN). Monokine induction of ACH-2 cells resulted in augmented virus production reflected by an increase in reverse transcriptase activity and in the synthesis of all major viral proteins. Examination of the cells by indirect immunofluorescence revealed that 10 to 15% of uninduced cells constitutively expressed HIV proteins, whereas 100% showed positive immunofluorescence in response to LPS-MO SN. This induction of virus by LPS-MO SN resulted in approximately a 100-fold increase of infectious virus production over uninduced ACH-2 cells. LPS alone could not induce HIV-1 expression, whereas LPS-MO SN resulted in the greatest virus expression. Cell separation studies confirmed the source of the inducing factor(s) to be cells bearing the mature monocyte/macrophage marker, Leu M3. Biochemical fractionation of the LPS-MO SN suggested that one or more factors, having apparent Mr of approximately 45 kDa, were involved in this induction. Absorption of the LPS-MO SN with immunoaffinity gels specific for human TNF-alpha was shown to completely remove the HIV inducing activity for the ACH-2 cell line.