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Open Access Research

Regulation of the HIV-1 promoter by HIF-1α and Vpr proteins

Satish L Deshmane1, Shohreh Amini13, Satarupa Sen1, Kamel Khalili1 and Bassel E Sawaya2*

Author Affiliations

1 Center for Neurovirology, Department of Neuroscience, Temple University School of Medicine, 3500 N. Broad Street, Philadelphia, PA 19140, USA

2 Molecular Studies of Neurodegenerative Diseases Laboratory - Department of Neurology, Temple University School of Medicine, 3420 N. Broad Street, Philadelphia, PA 19140, USA

3 Department of Biology, College of Science and Technology, Temple University, 1900 N. 12th Street, Philadelphia, PA 19122, USA

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Virology Journal 2011, 8:477  doi:10.1186/1743-422X-8-477

Published: 24 October 2011


We previously demonstrated the ability of HIV-1 Vpr protein to activate the oxidative stress pathway, thus leading to the induction of the hypoxia inducible factor 1 alpha (HIF-1α). Therefore, we sought to examine the interplay between the two proteins and the impact of HIF-1α activation on HIV-1 transcription. Using transient transfection assays, we identified the optimal concentration of HIF-1α necessary for the activation of the HIV-1 promoter as well as the domain within HIF-1α responsible for this activation. Our findings indicated that activation of the HIV-1 LTR by Vpr is HIF-1α dependent. Furthermore, we showed that both Vpr and HIF-1α activate the HIV-1 promoter through the GC-rich binding domain within the LTR. Taken together, these data shed more light on the mechanisms used by Vpr to activate the HIV-1 promoter and placed HIF-1α as a major participant in this activation.