Role of Chromatin Remodeling in HIV Transcription
Shweta Hakre, The J. David Gladstone Institutes, San Francisco
Mentor: Eric Verdin
Training in Basic Biomedical Sciences
Postdoctoral Fellowship Award
2009
The HIV-1 genome integrates itself into the host genome and productively infects the host cells. Most of the cells infected by HIV are productively infected. However, there is a small pool of cells that contain an integrated DNA that is transcriptionally silent (latent). This reservoir has the capacity to be restimulated and produce infectious virus. These latent cells remain to be of great clinical importance since they serve as a source of virus that has the capability of entering the infectious pool upon cessation of HAART. HIV latency is regulated at the level of proviral transcription. In order to understand HIV latency at the molecular level, my project involves the study of complexes that possibly control cellular latency (repression) of the HIV promoter at the chromatin level. These complexes have been documented to be the SWI/SNF complexes. My project will further characterize the molecular role of individual SWI/SNF complexes (namely the BAF and PBAF complex) in regulating HIV transcription. We expect that insights gathered from these studies will help to serve as essential tools in understanding the biology and therapy for HIV latency.
