Important note: Information in this article was accurate in July 2007. The state of the art may have changed since the publication date.
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AIDSWEEKLY Plus; Monday, July 30, 2007
Staff Medical Writers
Human immunodeficiency virus type 1 (HIV-1) causes AIDS by depleting essential immune cells called CD4+T lymphocytes in infected individuals, resulting in a compromised immune system. At the center of this process is the HIV protein, viral protein R (Vpr), which stops infected CD4+T cells from dividing and as a consequence compromises their immune function. In addition, by arresting cell division, Vpr helps HIV to harness the infected cell’s resources to enhance viral replication. The way Vpr exerts this effect is by interacting with cellular proteins that control cell division.
Dr. Cohen and his team have identified a novel cellular protein complex targeted by HIV-1 Vpr to stop infected cell division. This protein complex, designated DDB1-CUL4-VprBP, is involved in a process called ubiquitination. Ubiquitination is a mechanism by which a small protein called ubiquitin is conjugated to cellular proteins in order to modulate their biological activity or induce their degradation. The researchers demonstrated that association of Vpr with this ubiquitinating complex, also called an E3 ubiquitin ligase complex, is essential for the defect in cell division induced by Vpr. Further characterization of this protein complex as well as the elucidation of the mechanism by which it affects cell division may open new avenues for therapeutic intervention against HIV.
Keywords: HIV/AIDS, AIDS, Acquired Immunodeficiency Syndrome, HIV, Human Immunodeficiency Virus, Viral, Virology, Institut de recherches cliniques de Montréal.
This article was prepared by AIDS Weekly editors from staff and other reports.
Reference
Jean-Philippe Belzile, Ghislaine Duisit, Nicole Rougeau, et al., HIV-1 Vpr-Mediated G2 Arrest Involves the DDB1-CUL4AVPRBP E3 Ubiquitin Ligase, PLoS Pathog 2007 Jul 13;3(7): e85.
2007-07-30
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