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Research Article Free access | 10.1172/JCI117924

Mycobacterium tuberculosis enhances human immunodeficiency virus-1 replication by transcriptional activation at the long terminal repeat.

Y Zhang, K Nakata, M Weiden, and W N Rom

Department of Medicine, New York University Medical Center, New York 10016, USA.

Find articles by Zhang, Y. in: PubMed | Google Scholar

Department of Medicine, New York University Medical Center, New York 10016, USA.

Find articles by Nakata, K. in: PubMed | Google Scholar

Department of Medicine, New York University Medical Center, New York 10016, USA.

Find articles by Weiden, M. in: PubMed | Google Scholar

Department of Medicine, New York University Medical Center, New York 10016, USA.

Find articles by Rom, W. in: PubMed | Google Scholar

Published May 1, 1995 - More info

Published in Volume 95, Issue 5 on May 1, 1995
J Clin Invest. 1995;95(5):2324–2331. https://doi.org/10.1172/JCI117924.
© 1995 The American Society for Clinical Investigation
Published May 1, 1995 - Version history
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Abstract

Tuberculosis has emerged as an epidemic fueled by the large number of individuals infected with the human immunodeficiency virus, especially those who are injecting drug users. We found a striking increase from 4- to 208-fold in p24 levels in bronchoalveolar lavage fluid from involved sites of Mycobacterium tuberculosis infection vs uninvolved sites in three HIV+ patients. We used an in vitro cell culture model to determine if tuberculosis could activate replication of HIV-1. Mononuclear phagocyte cell lines U937 and THP-1 infected with HIV-1JR-CSF, in vitro and stimulated with live M. tuberculosis H37Ra, had a threefold increase in p24 in culture supernatants. Using the HIV-1 long terminal repeat with a chloramphenicol acetyltransferase (CAT) reporter construct, live M. tuberculosis increased transcription 20-fold in THP-1 cells, and cell wall components stimulated CAT expression to a lesser extent. The nuclear factor-kappa B enhancer element was responsible for the majority of the increased CAT activity although two upstream nuclear factor-IL6 sites may also contribute to enhanced transcription. Antibodies to TNF-alpha and IL-1 inhibited the increase in CAT activity of the HIV-1 long terminal repeat by M. tuberculosis from 21-fold to 8-fold. Stimulation of HIV-1 replication by M. tuberculosis may exacerbate dysfunction of the host immune response in dually infected individuals.

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