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Corrigendum Free access | 10.1172/JCI151380

The multifaceted nature of HIV latency

Caroline Dufour, Pierre Gantner, Rémi Fromentin, and Nicolas Chomont

Find articles by Dufour, C. in: JCI | PubMed | Google Scholar

Find articles by Gantner, P. in: JCI | PubMed | Google Scholar

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

Find articles by Chomont, N. in: JCI | PubMed | Google Scholar

Published June 1, 2021 - More info

Published in Volume 131, Issue 11 on June 1, 2021
J Clin Invest. 2021;131(11):e151380. https://doi.org/10.1172/JCI151380.
© 2021 American Society for Clinical Investigation
Published June 1, 2021 - Version history
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The multifaceted nature of HIV latency
Caroline Dufour, … , Rémi Fromentin, Nicolas Chomont
Caroline Dufour, … , Rémi Fromentin, Nicolas Chomont
Review Series

The multifaceted nature of HIV latency

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Abstract

Although antiretroviral therapies (ARTs) potently inhibit HIV replication, they do not eradicate the virus. HIV persists in cellular and anatomical reservoirs that show minimal decay during ART. A large number of studies conducted during the past 20 years have shown that HIV persists in a small pool of cells harboring integrated and replication-competent viral genomes. The majority of these cells do not produce viral particles and constitute what is referred to as the latent reservoir of HIV infection. Therefore, although HIV is not considered as a typical latent virus, it can establish a state of nonproductive infection under rare circumstances, particularly in memory CD4+ T cells, which represent the main barrier to HIV eradication. While it was originally thought that the pool of latently infected cells was largely composed of cells harboring transcriptionally silent genomes, recent evidence indicates that several blocks contribute to the nonproductive state of these cells. Here, we describe the virological and immunological factors that play a role in the establishment and persistence of the pool of latently infected cells and review the current approaches aimed at eliminating the latent HIV reservoir.

Authors

Caroline Dufour, Pierre Gantner, Rémi Fromentin, Nicolas Chomont

×

Original citation: J Clin Invest. 2020;130(7):3381–3390. https://doi.org/10.1172/JCI136227

Citation for this corrigendum: J Clin Invest. 2021;131(11):e151380. https://doi.org/10.1172/JCI151380

The description of the effect of polypyrimidine tract–binding protein (PTB) on HIV RNA export was incorrect in the section Molecular mechanisms of HIV latency and in Figure 3.

The correct sentence is below.

Furthermore, viral RNAs accumulate in the nucleus of latently infected cells, and this defect in RNA export can be reverted by overexpressing the polypyrimidine tract–binding protein (PTB) in resting cells (39).

The text and Figure 3 have been updated in the HTML version and PDF with the correct information.

The authors regret the error.

Footnotes

See the related article at The multifaceted nature of HIV latency.

Version history
  • Version 1 (June 1, 2021): Electronic publication

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