Mechanisms that contribute to HIV latency

Published in the June issue of Cell Host & Microbe, Marina Lusic and colleagues in the Molecular Medicine lab explore mechanisms that contribute to HIV latency.

As stated in the Editor's choice in the July 5 issue of Science, "The ability of HIV to reside in a latent form in T cells is a major hurdle to finding a cure. With no widely protective vaccine on the horizon, there is growing interest in understanding how to convert latent HIV into a replication active state, which would allow therapies that target infected cells to eliminate them. Mechanisms that contribute to HIV latency, however, are poorly understood. Using a combination of immuno-3D fluorescent in situ hybridization and chromatin immunoprecipitation, Lusic et al. find that location matters for latency."

In investigating the mechanisms mediating HIV-1 latency, the team determined that silenced but transcriptionally competent HIV-1 proviruses reside in close proximity to PML NBs and that this association inhibits HIV-1 gene expression. Thus, nuclear topology and active gene movement mediate HIV-1 transcriptional regulation and have implications for controlling HIV-1 latency and eradication.

Related articles:

5 July 2013
Science, vol 341, Editors' Choice: Location, Location, Location

12 June 2013
Cell Host & Microbe 13, Previews: Three Rules for HIV Latency: Location, Location, and Location

Cell Host & Microbe 13, 665-77 Lusic M. et al: Proximity to PML nuclear bodies regulates HIV-1 latency in CD4+ T cells (link to PubMed)


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