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Tumor necrosis factor alpha induces expression of human immunodeficiency virus in a chronically infected T-cell clone.

Proceedings of the National Academy of SciencesPublished 1 April 1989Open access
T M Folks, Kathleen A. Clouse, J. Shawn Justement, Arnold B. Rabson, Elia J. Duh, John H. Kehrl
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TL;DR

Transient-transfection experiments demonstrated that the inductive effects of TNF-alpha were due to specific activation of the HIV long terminal repeat, providing evidence that T NF-alpha may play a role in the mechanisms of pathogenesis of HIV infection.

Abstract

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.

Keywords

Immunology and Microbiology