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
Current Drug Targets - Immune, Endocrine & Metabolic Disorders
Title: Blocking HIV-1 Vif Restores a Natural Mechanism of Intracellular Antiviral Defense
Volume: 4 Issue: 4
Author(s): Chiara Bovolenta
Affiliation:
Keywords: vif, f12-vif, apobec3g, apobec3f, hiv-1, anti-viral therapy, non-immune defense
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.
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Cite this article as:
Bovolenta Chiara, Blocking HIV-1 Vif Restores a Natural Mechanism of Intracellular Antiviral Defense, Current Drug Targets - Immune, Endocrine & Metabolic Disorders 2004; 4 (4) . https://dx.doi.org/10.2174/1568005310404040257
DOI https://dx.doi.org/10.2174/1568005310404040257 |
Print ISSN 1568-0088 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5917 |
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