Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2006-10-27
pubmed:abstractText
Members of the APOBEC family of cellular polynucleotide cytidine deaminases (e.g., APOBEC3G) are potent inhibitors of HIV infection. Wild type viral infections are largely spared from APOBEC function through the action of the viral Vif protein. In Vif's absence, inhibitory APOBEC proteins are encapsidated by budding virus particles leading to excessive cytidine (C) to uridine (U) hypermutation of negative sense reverse transcripts in newly infected cells. This registers as guanosine (G) to adenosine (A) mutations in plus stranded cDNA. Because the functions of Vif and APOBEC proteins oppose each other, it is likely that fluctuations in the Vif/APOBEC balance can influence the natural history of HIV infection. Experimental support for this notion would further justify and stimulate drug discovery initiatives in this area.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1631-0691
pubmed:author
pubmed:issnType
Print
pubmed:volume
329
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
871-5
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Natural resistance to HIV infection: The Vif-APOBEC interaction.
pubmed:affiliation
Department of Infectious Diseases, King's College London, School of Medicine, 2nd Floor, New Guy's House, Guy's Hospital, London Bridge, London SE1 9RT, UK. michael.malim@kcl.ac.uk
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't