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

HIV-1 Vpr enhances production of receptor of activated NF-κB ligand (RANKL) via potentiation of... 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-κB 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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Virology Springer Journals

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

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Publisher
Springer Journals
Copyright
Copyright © 2005 by Springer-Verlag/Wien
Subject
Biomedicine; Medical Microbiology; Virology; Infectious Diseases
ISSN
0304-8608
eISSN
1432-8798
D.O.I.
10.1007/s00705-004-0395-7
Publisher site
See Article on Publisher Site

Abstract

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-κB 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.

Journal

Archives of VirologySpringer Journals

Published: Jan 1, 2005

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