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Review
.2008 Sep;6(5):388-400.
doi: 10.2174/157016208785861195.

Cellular reservoirs of HIV-1 and their role in viral persistence

Affiliations
Review

Cellular reservoirs of HIV-1 and their role in viral persistence

Aikaterini Alexaki et al. Curr HIV Res.2008 Sep.

Abstract

A major obstacle in human immunodeficiency virus type 1 (HIV-1) eradication is the ability of the virus to remain latent in a subpopulation of the cells it infects. Latently infected cells can escape the viral immune response and persist for long periods of time, despite the presence of successful highly active antiretroviral therapy (HAART). Given the appropriate stimulus, latently infected cells can reactivate and start producing infectious virions. The susceptibility of these cell populations to HIV-1, their life span, their proliferative capacity, and their ability to periodically produce infectious virus subsequent to alterations in cellular physiology and/or immunologic controls are critical issues which determine the contribution of these cells to viral persistence. Memory CD4+ T cells due to the long life span, which may be several years, and their ability to reactivate upon encounter with their cognate antigen or other stimulation, are considered a critical reservoir for maintenance of latent HIV-1 proviral DNA. Cells of the monocyte-macrophage lineage, which originate in the bone marrow (BM), are of particular importance in HIV-1 persistence due to their ability to cross the blood-brain barrier (BBB) and spread HIV-1 infection in the immunoprivileged central nervous system (CNS). Hematopoietic progenitor cells (HPCs) are also a potential HIV-1 reservoir, as several studies have shown that CD34+ HPCs carrying proviral DNA can be found in vivo in a subpopulation of HIV-1-infected patients. The ability of HPCs to proliferate and potentially generate clonal populations of infected cells of the monocyte-macrophage lineage may be crucial in HIV-1 dissemination. The contribution of these and other cell populations in HIV-1 persistence, as well as the possible strategies to eliminate latently infected cells are critically examined in this review.

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Figures

Fig. (1)
Fig. (1). Activation of integrated HIV-1 LTR
Integration of HIV-1 DNA into heterochromatin may suppress viral gene expression (A). Several stimuli, including TCR engagement in CD4+ T cells (B), and proinflammatory cytokine stimulation in monocyte-macrophages (C), induce signaling cascades that may ultimately lead to changes in the nuclear transcription factor milieu. Although available and induced transcription factors may differ between CD4+ T cells and cells of the monocyte-macrophage lineage, in both cases they facilitate histone methylation and acetylation that may promote conversion of heterochromatin to euchromatin. Cumulatively, these changes may allow viral gene expression and emergence from latency (D).
Fig. (2)
Fig. (2). Cellular HIV-1 reservoirs in the lymph nodes
Lymph nodes are a site of pronounced viral production. The majority of virions are being produced by activated T cells but DCs and resting T cells may also be infected. Interaction of resting T cells with their autologous DCs or B cells, or with follicular dendritic cells may render them permissive to HIV-1 infection.
Fig. (3)
Fig. (3). Cellular HIV-1 reservoirs in the CNS
Perivascular macrophages and microglia are the major HIV-1 producing cells in the CNS. HIV-1 infection of astrocytes is considered to be non-productive.
Fig. (4)
Fig. (4). Cellular HIV-1 reservoirs in the blood
In addition to CD4+ T cells and monocytes, infected mast cells and potentially NK cells may also be present in the blood of HIV-1-infected patients.
See this image and copyright information in PMC

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