Open AccessHuman APOBEC3G-Mediated Editing Can Promote HIV-1 Sequence Diversification and Accelerate Adaptation to Selective Pressure
Author(s) -
Eun Young Kim,
Tanmoy Bhattacharya,
Kevin Kunstman,
Peter Swantek,
F. Koning,
Michael H. Malim,
Steven M. Wolinsky
Publication year - 2010
Publication title -
journal of virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.617
H-Index - 292
eISSN - 1070-6321
pISSN - 0022-538X
DOI - 10.1128/jvi.01223-10
Subject(s) - apobec3g , cytidine deaminase , biology , genetics , virology , cytidine , viral replication , virus , apobec , activation induced (cytidine) deaminase , enzyme , gene , somatic hypermutation , biochemistry , antibody , b cell , genome
Human apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3G (APOBEC3G, hereinafter referred to as A3G) is an innate virus restriction factor that inhibits human immunodeficiency virus type 1 (HIV-1) replication and induces excessive deamination of cytidine residues in nascent reverse transcripts. To test the hypothesis that this enzyme can also help generate viral sequence diversification and the evolution of beneficial viral variants, we have examined the impact of A3G on the acquisition of (−)2′,3′-dideoxy-3′-thiacytidine (3TC) resistancein vitro . That characteristic resistance mutations are rapidly fixed in the presence of A3G and 3TC suggests that A3G-mediated editing can be an important source of genetic variation on which natural selection acts to shape the structure of HIV-1 populations.