HIV-1 Infection Explained

The T cells are destroyed by HIV viral protein Vpr. This protein regulates a variety of cellular functions, including cell death, immune suppression and inhibition of cell proliferation.

One of the ways Vpr exerts its effects is by binding to a T-cell steroid hormone receptor (GR). David B. Weiner and colleagues from the University of Pennsylvania show that through binding to GR, Vpr keeps a crucial co-activator of gene expression, PARP-1, away from it's target, thus blocking an essential survival pathway Vpr induces binding of PARP-1 to GR, thus preventing PARP-1 from activating expression of essential survival genes. Importantly, when GR is normally activated by its steroid hormone, binding of PARP-1 to GR does not occur, indicating that the association of these two molecules is directly mediated by the viral protein Vpr, during HIV-1 infection. Understanding the molecular mechanism that depletes T cells and consequently affects the immune system may open new avenues for therapeutic intervention against HIV-1.

Author Contact:

David B. Weiner (Dept of Pathology and Lab. Medicine, University of Pennsylvania, PA, USA).
E-mail: dbweiner@mail.med.upenn.edu

Abstract available online.

(C) Nature Cell Biology press release.

Message posted by: Trevor M. D'Souza