Commentary 10.1172/JCI95329

HIV persistence: clonal expansion of cells in the latent reservoir

Kyungyoon J. Kwon1 and Robert F. Siliciano1,2

1Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.

2Howard Hughes Medical Institute, Baltimore, Maryland, USA.

Address correspondence to: Robert F. Siliciano, Room 879, Edward D. Miller Research Building, 733 N. Broadway, Baltimore, Maryland 21205, USA. Phone: 410.955.2958; Email: rsiliciano@jhmi.edu.

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

1Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.

2Howard Hughes Medical Institute, Baltimore, Maryland, USA.

Address correspondence to: Robert F. Siliciano, Room 879, Edward D. Miller Research Building, 733 N. Broadway, Baltimore, Maryland 21205, USA. Phone: 410.955.2958; Email: rsiliciano@jhmi.edu.

Find articles by Siliciano, R. in: JCI | PubMed | Google Scholar

First published June 19, 2017 - More info

Published in Volume 127, Issue 7 (June 30, 2017)
J Clin Invest. 2017;127(7):2536–2538. doi:10.1172/JCI95329.
Copyright © 2017, American Society for Clinical Investigation

First published June 19, 2017

See the related article at Clonal expansion of genome-intact HIV-1 in functionally polarized Th1 CD4+ T cells.

While antiretroviral therapy (ART) can reduce HIV-1 to undetectable levels, the virus generally reappears if treatment is stopped. Resurgence of the virus is due to the reactivation of T cells harboring latent integrated provirus, and recent studies indicate that proliferation of these latently infected cells helps maintain the HIV-1 reservoir. In this issue of the JCI, Lee et al. evaluated CD4+ T cell subsets to determine whether certain populations are more likely to harbor full-length, replication-competent provirus. The authors identified an enrichment of clonally expanded Th1 cells containing intact HIV-1 proviruses, suggesting that this polarized subset contributes to the persistence of the reservoir. Strategies to target these provirus-harboring cells need to be considered for future therapies aimed toward HIV-1 cure.

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