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

T. M. Folks, K. A. Clouse, J. Justement, A. Rabson, E. Duh, J. H. Kehrl, A. S. Fauci

Research output: Contribution to journalArticlepeer-review

Abstract

Tumor necrosis factor α (TNF-α), 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-α 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-α 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-α. Transient-transfection experiments demonstrated that the inductive effects of TNF-α were due to specific activation of the HIV long terminal repeat. These studies provide evidence that TNF-α may play a role in the mechanisms of pathogenesis of HIV infection.

Original languageEnglish (US)
Pages (from-to)2365-2368
Number of pages4
JournalProceedings of the National Academy of Sciences of the United States of America
Volume86
Issue number7
DOIs
StatePublished - 1989
Externally publishedYes

ASJC Scopus subject areas

  • General

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