Blocking HIV-1 Vif Restores a Natural Mechanism of Intracellular Antiviral Defense | Bentham Science
Generic placeholder image

Current Drug Targets - Immune, Endocrine & Metabolic Disorders

Editor-in-Chief

ISSN (Print): 1568-0088
ISSN (Online): 1875-5917

Blocking HIV-1 Vif Restores a Natural Mechanism of Intracellular Antiviral Defense

Author(s): Chiara Bovolenta

Volume 4, Issue 4, 2004

Page: [257 - 263] Pages: 7

DOI: 10.2174/1568005310404040257

Price: $65

Open Access Journals Promotions 2
Abstract

AIDS has become the greatest pandemic in the human history counting approximately 40 millions people worldwide. To purge HIV-1 infection, new therapeutic approaches need to be searched in alternative and / or in addition to the current pharmacological ones. Recently, several independent laboratories have unveiled a nonimmune intracellular anti-HIV-1 defense strategy based on the cytidine deaminase APOBEC3G, which restricts HIV- 1 production by directly mutating the proviral DNA in infected cells. To counteract this defense pathway, HIV-1 has developed an evasion strategy by acquiring the accessory protein Vif, which blocks the action of APOBEC3G by inducing its proteasome-mediated degradation.

Keywords: vif, f12-vif, apobec3g, apobec3f, hiv-1, anti-viral therapy, non-immune defense

Next »

Rights & Permissions Print Cite
© 2024 Bentham Science Publishers | Privacy Policy