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The multifaceted nature of HIV latency
Caroline Dufour, … , Rémi Fromentin, Nicolas Chomont
Caroline Dufour, … , Rémi Fromentin, Nicolas Chomont
Published July 1, 2020
Citation Information: J Clin Invest. 2020;130(7):e136227. https://doi.org/10.1172/JCI136227.
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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

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Figure 2

Models for the establishment of HIV latency.

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Models for the establishment of HIV latency.
Postactivation latency refe...
Postactivation latency refers to a phenomenon by which activated productively infected CD4+ T cells revert back to a quiescent state, which is accompanied by the silencing of the HIV promoter. In preactivation latency, resting CD4+ T cells, which are usually refractory to HIV infection, become permissive and establish latency directly (i.e., in the absence of T cell activation).

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