In vivo, in vitro, and in silico analysis of methylation of the HIV-1 provirus.

Leonard Chávez, Steven Kauder, Eric Verdin

Journal: Methods (San Diego, Calif.) 2011;53(1):47-53

PMID: 20670606

Abstract

HIV-1 latency is a barrier to overcome in the effort to fully eradicate the virus from infected individuals using highly active anti-retroviral therapy (HAART). Therefore, the study of the mechanisms underlying the establishment and maintenance of HIV-1 latency are vital to achieving a cure. Transcriptional repression of the viral promoter is the major cause of HIV-1 latency. DNA methylation of genomic regions known as CpG islands (CpGIs) is a well-established transcriptional regulatory mechanism, and the HIV-1 provirus contains several conserved CpGIs including two that are located within the viral promoter region. The study of these CpGIs in both in vitro and in vivo models of HIV-1 latency using the technique of bisulfite-mediated methylcytosine mapping has led to their identification as factors that contribute to the maintenance of HIV-1 latency. Here, we discuss the identification of CpGIs within the HIV-1 provirus and the study of their differential methylation patterns in several HIV-1 latency models using bisulfite-mediated methylcytosine mapping.

Copyright © 2010 Elsevier Inc. All rights reserved.

Address: Gladstone Institute of Virology and Immunology, University of California, San Francisco, 1650 Owens Street, CA 94158-2261, USA. [email protected]
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