Vif and Apobec3G in the innate immune response to HIV: a tale of two proteins
Document Type
Journal ArticlePublication Date
2008-03-28Keywords
Cytidine Deaminase; HIV; HIV Infections; Humans; *Immunity, Innate; Models, Biological; vif Gene Products, Human Immunodeficiency VirusLife Sciences
Medicine and Health Sciences
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Show full item recordAbstract
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.Source
Future Microbiol. 2008 Apr;3:145-54. Link to article on publisher's siteDOI
10.2217/17460913.3.2.145Permanent Link to this Item
http://hdl.handle.net/20.500.14038/32919PubMed ID
18366335Related Resources
Link to Article in PubMedae974a485f413a2113503eed53cd6c53
10.2217/17460913.3.2.145