Linked Life Data

18366335

Source:http://linkedlifedata.com/resource/pubmed/id/18366335

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2008-3-27
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1746-0921
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
3
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
145-54
pubmed:dateRevised
2010-12-30
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Vif and Apobec3G in the innate immune response to HIV: a tale of two proteins.
pubmed:affiliation
College of the Holy Cross, Department of Biology, 1 College Street, Worcester, MA 01610, USA. mfarrow@holycross.edu
pubmed:publicationType
Journal Article, Review