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Vif and Apobec3G in the innate immune response to HIV: a tale of two proteins

dc.contributor.authorFarrow, Melissa Ann
dc.contributor.authorSheehy, Ann M.
dc.date2022-08-11T08:08:52.000
dc.date.accessioned2022-08-23T16:10:23Z
dc.date.available2022-08-23T16:10:23Z
dc.date.issued2008-03-28
dc.date.submitted2009-02-23
dc.identifier.citationFuture Microbiol. 2008 Apr;3:145-54. <a href="http://dx.doi.org/10.2217/17460913.3.2.145">Link to article on publisher's site</a>
dc.identifier.issn1746-0921 (Electronic)
dc.identifier.doi10.2217/17460913.3.2.145
dc.identifier.pmid18366335
dc.identifier.urihttp://hdl.handle.net/20.500.14038/32919
dc.description.abstractIt is now 26 years after the first published report on HIV, and the global epidemic continues unabated, with estimates of over 33 million people currently infected, worldwide. Development of targeted therapies aimed at perturbing the HIV life cycle can be achieved only with a detailed comprehension of the dynamics of virus-host interactions within the cell. One such critical virus-host interaction is the recently elucidated interplay between the viral Vif protein and the innate immune defense molecule Apobec3G. Apobec3G potently suppresses HIV replication, but Vif can alleviate this inhibition, rescuing viral infectivity. Early work describing the characterization of Vif and the cloning and identification of Apobec3G as an antiviral are discussed. Recent advances detailing the mechanisms of the Vif-Apobec3G regulatory circuit and our nascent understanding of Apobec3G endogenous function are also presented. Collectively, these studies have shed light on potential novel therapeutic strategies aimed at exploiting Apobec3G antiviral function to abrogate HIV replication.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=18366335&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.2217/17460913.3.2.145
dc.titleVif and Apobec3G in the innate immune response to HIV: a tale of two proteins
dc.typeJournal Article
dc.source.journaltitleFuture microbiology
dc.source.volume3
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/1470
dc.identifier.contextkey733767
html.description.abstract<p>It is now 26 years after the first published report on HIV, and the global epidemic continues unabated, with estimates of over 33 million people currently infected, worldwide. Development of targeted therapies aimed at perturbing the HIV life cycle can be achieved only with a detailed comprehension of the dynamics of virus-host interactions within the cell. One such critical virus-host interaction is the recently elucidated interplay between the viral Vif protein and the innate immune defense molecule Apobec3G. Apobec3G potently suppresses HIV replication, but Vif can alleviate this inhibition, rescuing viral infectivity. Early work describing the characterization of Vif and the cloning and identification of Apobec3G as an antiviral are discussed. Recent advances detailing the mechanisms of the Vif-Apobec3G regulatory circuit and our nascent understanding of Apobec3G endogenous function are also presented. Collectively, these studies have shed light on potential novel therapeutic strategies aimed at exploiting Apobec3G antiviral function to abrogate HIV replication.</p>
dc.identifier.submissionpathgsbs_sp/1470
dc.contributor.departmentCollege of the Holy Cross
dc.contributor.departmentMorningside Graduate School of Biomedical Sciences
dc.source.pages145-54


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