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Arch Virol. 2005 Jan;150(1):67-78. Epub 2004 Sep 24.

HIV-1 Vpr enhances production of receptor of activated NF-kappaB ligand (RANKL) via potentiation of glucocorticoid receptor activity.

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  • 1Laboratory for AIDS Virus Research, Department of Medicine, Weill Medical College of Cornell University, New York, NY 10021, USA.


The HIV-1 accessory protein Vpr potentiates glucocorticoid (GC)-induced inhibition of a variety of immunologically important cytokines. We report the first instance of synergy between Vpr and GC in induction of a T cell cytokine, one which may underlie a metabolic complication of HIV infection. Accelerated bone resorption is an important complication of HIV disease and its treatment. Receptor of activated NF-kappaB ligand (RANKL) is the final effector of osteoclast differentiation and bone resorption. It is induced by exogenous GC, a prominent cofactor in bone mineral loss, as well as by elevated levels of endogenous GC, found in many patients with HIV disease. We document Vpr-mediated upregulation of RANKL, the dependence of this effect on GC receptor integrity, its function through a classic GC receptor motif, and its independence from Vpr-mediated G(2) cell cycle arrest. These data suggest a positive regulatory role for Vpr in transcriptional control of a cytokine that may be critical to one metabolic complication of HIV.

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