Interleukin 6 induces human immunodeficiency virus expression in infected monocytic cells alone and in synergy with tumor necrosis factor alpha by transcriptional and post-transcriptional mechanisms.

Guido Poli(National Institute of Allergy and Infectious Diseases), Peter Bressler(National Institute of Allergy and Infectious Diseases), Audrey Kinter(National Institute of Allergy and Infectious Diseases), Elia J. Duh(National Institute of Allergy and Infectious Diseases), William C. Timmer(National Institute of Allergy and Infectious Diseases), Arnold B. Rabson(National Institute of Allergy and Infectious Diseases), J. Shawn Justement(National Institute of Allergy and Infectious Diseases), Sharilyn K. Stanley(National Institute of Allergy and Infectious Diseases), Anthony S. Fauci(National Institute of Allergy and Infectious Diseases)
The Journal of Experimental Medicine
July 1, 1990
Cited by 523Open Access
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Abstract

The immunoregulatory cytokine interleukin 6 (IL-6) directly upregulates production of human immunodeficiency virus (HIV) in acutely as well as in chronically infected cells of monocytic lineage. In addition, IL-6 synergizes with tumor necrosis factor alpha (TNF-alpha) in the induction of latent HIV expression. Unlike TNF-alpha, upregulation of viral expression induced by IL-6 alone does not occur at the transcriptional level and it is not associated with accumulation of HIV RNA. However, when IL-6 and TNF-alpha synergistically stimulate HIV production, accumulation of HIV RNA and increased transcription are observed, indicating that IL-6 affects HIV expression at multiple (transcriptional and post-transcriptional) levels.


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