Optimal Translation Initiation Enables Vif-Deficient Human Immunodeficiency Virus Type 1 To Escape Restriction by APOBEC3G

被引：26

作者：

Hache, Guylaine ^{[1
,2
,3
]}

Abbink, Truus E. M. ^{[4
]}

Berkhout, Ben ^{[5
]}

Harris, Reuben S. ^{[1
,2
,3
]}

机构：

[1] Univ Minnesota, Dept Biochem Mol Biol & Biophys, Minneapolis, MN 55455 USA

[2] Univ Minnesota, Inst Mol Virol, Minneapolis, MN 55455 USA

[3] Univ Minnesota, Ctr Genome Engn, Minneapolis, MN 55455 USA

[4] Univ Cambridge, Dept Med, Cambridge, England

[5] Univ Amsterdam, Lab Expt Virol, Acad Med Ctr, NL-1012 WX Amsterdam, Netherlands

来源：

JOURNAL OF VIROLOGY | 2009年 / 83卷 / 11期

基金：

美国国家卫生研究院;

关键词：

MURINE LEUKEMIA-VIRUS; REVERSE TRANSCRIPTION; ANTIVIRAL ACTIVITY; SITE; DEGRADATION; PROTEIN; REPLICATION; MECHANISM; INFECTION; CEM15;

D O I：

10.1128/JVI.00045-09

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

APOBEC3G restricts Vif-deficient human immunodeficiency virus type 1 (HIV-1) by deaminating viral cDNA cytosines to uracils. This promutagenic activity is counteracted by HIV-1 Vif, which is a natural APOBEC3G antagonist. However, we previously reported that Vif-deficient HIV-1 could evolve resistance to APOBEC3G by a novel mechanism requiring an A200-to-C/T transition mutation and Vpr inactivation. A pyrimidine at nucleotide 200 in the untranslated leader region contributed to resistance by increasing virus particle production, which resulted in fewer APOBEC3G molecules per particle. Here we show that the A200-to-C/T mutation functions posttranscriptionally by inactivating an upstream start codon, which in turn enables optimal viral mRNA translation from canonical start codons.

引用

页码：5956 / 5960

页数：5

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