Abstract
Vif is an HIV accessory protein whose primary function is to negate the action of APOBEC3G, a naturally occurring cellular inhibitor of HIV replication. Vif acts by binding to APOBEC3G, inducing its protein degradation within infected cells and reducing its levels in progeny virions. Interventions that interfere with the Vif-APOBEC3G interaction, raise intracellular or virion associated levels of APOBEC3G, or reduce intracellular levels of Vif, all could hold promise as potential therapeutic approaches aimed at enhancing the cells innate antiviral activity. Levels of APOBEC3G might be increased or Vif levels decreased, by strategies targeting protein synthesis, protein degradation or cellular localisation and function, and properties of APOBEC3G and Vif relevant to these strategies are discussed. Recent data have suggested that Vif may have other mechanisms of action apart from the above activities against APOBEC3G, including effects against other anti-viral mechanisms independent of APOBEC3G cytidine deaminase activity. In addition to interaction with APOBEC3G, Vif may have other accessory functions, which are discussed in relation to potential therapies that may affect multiple stages of the HIV life cycle. Future development of strategies that combine enhancement of APBOEC3G functional with inhibition of multiple Vif functions may become useful tools for HIV therapy.
Keywords: Vif, APOBEC3G, HIV, viral accessory protein, anti-viral therapy, cellular inhibitor, ZIN, reverse transcription
Current Drug Targets
Title: Cellular Interactions of Virion Infectivity Factor (Vif) as Potential Therapeutic Targets: APOBEC3G and More?
Volume: 7 Issue: 12
Author(s): J. M. Carr, A. J. Davis, F. Feng, C. J. Burrell and P. Li
Affiliation:
Keywords: Vif, APOBEC3G, HIV, viral accessory protein, anti-viral therapy, cellular inhibitor, ZIN, reverse transcription
Abstract: Vif is an HIV accessory protein whose primary function is to negate the action of APOBEC3G, a naturally occurring cellular inhibitor of HIV replication. Vif acts by binding to APOBEC3G, inducing its protein degradation within infected cells and reducing its levels in progeny virions. Interventions that interfere with the Vif-APOBEC3G interaction, raise intracellular or virion associated levels of APOBEC3G, or reduce intracellular levels of Vif, all could hold promise as potential therapeutic approaches aimed at enhancing the cells innate antiviral activity. Levels of APOBEC3G might be increased or Vif levels decreased, by strategies targeting protein synthesis, protein degradation or cellular localisation and function, and properties of APOBEC3G and Vif relevant to these strategies are discussed. Recent data have suggested that Vif may have other mechanisms of action apart from the above activities against APOBEC3G, including effects against other anti-viral mechanisms independent of APOBEC3G cytidine deaminase activity. In addition to interaction with APOBEC3G, Vif may have other accessory functions, which are discussed in relation to potential therapies that may affect multiple stages of the HIV life cycle. Future development of strategies that combine enhancement of APBOEC3G functional with inhibition of multiple Vif functions may become useful tools for HIV therapy.
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Cite this article as:
Carr M. J., Davis J. A., Feng F., Burrell J. C. and Li P., Cellular Interactions of Virion Infectivity Factor (Vif) as Potential Therapeutic Targets: APOBEC3G and More?, Current Drug Targets 2006; 7 (12) . https://dx.doi.org/10.2174/138945006779025356
DOI https://dx.doi.org/10.2174/138945006779025356 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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