Human APOBEC3G-Mediated Editing Can Promote HIV-1 Sequence Diversification and Accelerate Adaptation to Selective Pressure

被引：95

作者：

Kim, Eun-Young ^{[2
]}

Bhattacharya, Tanmoy ^{[3
,4
]}

Kunstman, Kevin ^{[2
]}

Swantek, Peter ^{[2
]}

Koning, Fransje A. ^{[1
]}

Malim, Michael H. ^{[1
]}

Wolinsky, Steven M. ^{[2
]}

机构：

[1] Kings Coll London, Sch Med, Dept Infect Dis, London SE1 9RT, England

[2] Northwestern Univ, Div Infect Dis, Feinberg Sch Med, Chicago, IL 60611 USA

[3] Los Alamos Natl Lab, Los Alamos, NM 87545 USA

[4] Santa Fe Inst, Santa Fe, NM 87501 USA

来源：

JOURNAL OF VIROLOGY | 2010年 / 84卷 / 19期

基金：

美国国家卫生研究院; 英国医学研究理事会;

关键词：

IMMUNODEFICIENCY-VIRUS TYPE-1; DRUG-RESISTANCE; CYTIDINE DEAMINATION; ENZYME APOBEC3G; VIF PROTEIN; INFECTION; DNA; HYPERMUTATION; DEGRADATION; PATTERNS;

D O I：

10.1128/JVI.01223-10

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

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) resistance in 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.

引用

页码：10402 / 10405

页数：4

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