In vivo, in vitro, and in silico analysis of methylation of the HIV-1 provirus.
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.
Chávez
Leonard
L
Gladstone Institute of Virology and Immunology, University of California, San Francisco, 1650 Owens Street, CA 94158-2261, USA. leonard.chavez@ucsf.edu
Kauder
Steven
S
Verdin
Eric
E
D044503:5-Methylcytosine; D001483:Base Sequence; D003001:Cloning, Molecular; D003198:Computer Simulation; D018899:CpG Islands; D019175:DNA Methylation; D004279:DNA, Viral / Q000378:metabolism; D016679:Genome, Viral; D015658:HIV Infections / Q000235:genetics*; D015497:HIV-1 / Q000235:genetics / Q000502:physiology*; D006801:Humans; D008957:Models, Genetic; D011533:Proviruses / Q000235:genetics / Q000502:physiology*; D013447:Sulfites; D016662:Virus Integration; D017735:Virus Latency
D004279:DNA, Viral; D013447:Sulfites; D044503:5-Methylcytosine; C042345:hydrogen sulfite