An insight into the development of AIDS from HIV-1, is reported in the February issue of Nature Cell Biology. Human immunodeficiency virus type 1 (HIV-1) causes AIDS by depleting essential immune cells called T cells in infected individuals, resulting in a compromised immune system.
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.
David B. Weiner (Dept of Pathology and Lab. Medicine, University of Pennsylvania, PA, USA).
Abstract available online.
(C) Nature Cell Biology press release.
Message posted by: Trevor M. D'Souza
Bookmark and Share this page (what is this?)
Social bookmarking allows users to save and categorise a personal collection of bookmarks and share them with others. This is different to using your own browser bookmarks which are available using the menus within your web browser.
Use the links below to share this article on the social bookmarking site of your choice.
Read more about social bookmarking at Wikipedia - Social Bookmarking