A treatment called Highly Active Anti-Retroviral Therapy, or HAART, has proven very effective at suppressing HIV. However, in a very small number of infected T-cells the virus remains latent and inaccessible to treatment. Patients must receive HAART continuously—otherwise, the virus rebounds. The mechanism behind the persistence (and reactivation potential) of latent infected cells is not fully understood. In this study, the researchers uncovered the role of two enzymatic complexes called BAF and PBAF, which play distinct roles at different points in the HIV life cycle. BAF contributes to temporary suppression (and thus latency) of the virus by making key sites of the HIV genome inaccessible to the cellular machinery necessary for gene expression, thus silencing HIV transcription; PBAF, on the other hand, facilitates HIV transcription. The results point to a specific enzyme subunit of BAF, called BRG1, as a promising target for novel compounds designed to deplete the reservoir of latent HIV in infected patients.
PLos Biology. 2011 Nov;9(11):e1001206. Epub 2011 Nov 29. - http://www.ncbi.nlm.nih.gov/pubmed?term=22140357
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