DNA Methylation and HIV Latency

July 1st, 2009. You’d think keeping HIV from replicating was a good thing, and it is … unless you’re trying to eradicate the virus.
 
One of the world's most elusive viruses is an expert at maintaining a low profile, laying dormant in CD4+ cells even during highly active anti-retroviral treatment (HAART). A team of American and Swedish researchers found that the virus might be using DNA methylation as a cloak.

Hypermethylated CpG islands flanking the HIV transcription site attract methyl-CpG binding domain protein 2 (MBD2) -- an endogenous host protein – which in turn recruits histone deacetylaces and other enzymes to shut down transcription.
 
Using 5-aza-deoxycytidine (Aza-CdR) to strip the DNA methylation at these island allowed researchers to reverse the transcriptional block and reactivate HIV right out of hiding, indicating that Aza-CdR might be a great complement to other antiviral therapies. So there’s hope for flushing out the reservoir, clearing patients of HIV-1, and letting them live a drug free life. 

See all the details at PloS Pathogens June 2009.