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Current HIV/AIDS Reports

, Volume 7, Issue 1, pp 37–43 | Cite as

Mechanisms of HIV Latency: an Emerging Picture of Complexity

  • David M. Margolis
Article

Abstract

Rarely HIV type 1 establishes proviral latency within the host genome, maintained with little or no viral gene expression. This state has been quantitated in peripheral blood and lymphoid tissues of HIV-infected patients, appearing in the earliest days of infection. These rare cellular reservoirs are unaffected by current antiretroviral therapy and unrecognized by the host immune response, and can regenerate disseminated viremia if therapy is interrupted. Proviral latency may be established when a newly HIV-infected cell exits the cell cycle and returns to the resting state. Rarely, direct infection of resting cells may also occur. Multiple molecular mechanisms appear to underlie the establishment and maintenance of persistent, latent HIV infection, most frequent in the resting central memory CD4+ T cell. Interrupting processes that maintain latency may allow therapeutic attack of this primary form of persistent HIV infection, but a better understanding of relevant mechanisms in vivo is needed.

Keywords

Latency Resting CD4+ T cell Chromatin Histone HDAC Methylation IL-7 

Notes

Disclosure

Dr. Margolis has received research support from Merck Research Laboratories, who produce Vorinostat (suberoylanilide hydroxamic acid).

References

Papers of particular interest, published recently, have been highlighted as: • Of importance •• Of major importance

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Copyright information

© Springer Science+Business Media, LLC 2010

Authors and Affiliations

  1. 1.Departments of Medicine, Microbiology and Immunology, and EpidemiologyUniversity of North Carolina at Chapel HillChapel HillUSA

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