HIV latency: experimental systems and molecular models

FEMS Microbiol Rev. 2012 May;36(3):706-16. doi: 10.1111/j.1574-6976.2012.00335.x.


Highly active antiretroviral therapy (HAART) has shown great efficacy in increasing the survival of HIV infected individuals. However, HAART does not lead to the full eradication of infection and therefore has to be continued for life. HIV persists in a transcriptionally inactive form in resting T cells in HAART-treated patients and can be reactivated following T-cell activation. These latently infected cells allow the virus to persist in the presence of HAART. Here, we review recent advances in the study of the molecular mechanisms of HIV latency. We also review experimental models in which latency is currently studied. We focus on the epigenetic mechanisms controlling HIV transcription and on the role of chromatin and its post-translational modifications. We discuss how small molecule inhibitors that target epigenetic regulators, such as HDAC (histone deacetylase) inhibitors, are being tested for their ability to reactivate latent HIV. Finally, we discuss the clinical potential of these drugs to flush out latently infected cells from HIV-infected patients and to eradicate the virus.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Gene Expression Regulation, Viral
  • HIV / immunology*
  • HIV / pathogenicity*
  • HIV Infections / immunology*
  • HIV Infections / virology*
  • Host-Pathogen Interactions*
  • Humans
  • Models, Molecular
  • T-Lymphocytes / virology*
  • Virus Activation
  • Virus Latency*