TUMOR NECROSIS FACTOR-ALPHA INDUCES EXPRESSION OF HUMAN IMMUNODEFICIENCY VIRUS IN A CHRONICALLY INFECTED T-CELL CLONE
TUMOR NECROSIS FACTOR-ALPHA INDUCES EXPRESSION OF HUMAN IMMUNODEFICIENCY VIRUS IN A CHRONICALLY INFECTED T-CELL CLONE
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DOI：
10.1073/pnas.86.7.2365
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发表时间：
1989-04-01
影响因子：
11.1
通讯作者：
FAUCI, AS
中科院分区：
文献类型：
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作者：
FOLKS, TM;CLOUSE, KA;FAUCI, AS
肿瘤坏死因子α（TNF-α），也称为恶病质素，被证明在慢性感染的T细胞克隆（ACH-2）中诱导人免疫缺陷病毒（HIV）的表达。重组TNF-α的浓度如通过上清液逆转录酶活性所测定的，低至50 μ g/ml诱导ACH-2细胞中HIV表达的背景显著增加。TNF-α的HIV诱导作用无法用对细胞的毒性作用来解释。此外，未感染的亲本细胞系（A3.01）和感染的ACH-2细胞均显示具有TNF-α的高亲和力受体。瞬时转染实验证明TNF-α的诱导作用在细胞内表达。是由于HIV长末端重复序列的特异性激活。这些研究提供了TNF-α.可能在HIV感染的发病机制中发挥作用。
Tumor necrosis factor .alpha. (TNF-.alpha.), also known as cachectin, was demonstrated to induce the expression of human immunodeficiency virus (HIV) in a chronically infected T-cell clone (ACH-2). Concentrations of recombinant TNF-.alpha. as low as 50 pg/ml induced a significant increase over background of HIV expression in the ACH-2 cells as determined by supernatant reverse transcriptase activity. The HIV-inducing effects of TNF-.alpha. could not be explained by toxic effects on the cells. In addition, both the uninfected parental cell line (A3.01) and the infected ACH-2 cells were shown to have high-affinity receptors for TNF-.alpha.. Transient-transfection experiments demonstrated that the inductive effects of TNF-.alpha. were due to specific activation of the HIV long terminal repeat. These studies provide evidence that TNF-.alpha. may play a role in the mechanisms of pathogenesis of HIV infection.