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 language | English (US) |
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Pages (from-to) | 2365-2368 |
Number of pages | 4 |
Journal | Proceedings of the National Academy of Sciences of the United States of America |
Volume | 86 |
Issue number | 7 |
DOIs | |
State | Published - 1989 |
Externally published | Yes |
ASJC Scopus subject areas
- General