APOBEC3B Deletion and Risk of HIV-1 Acquisition

被引：47

作者：

An, Ping

Johnson, Randall

Phair, John ^{[5
]}

Kirk, Gregory D. ^{[2
]}

Yu, Xiao-Fang ^{[3
]}

Donfield, Sharyne ^{[6
]}

Buchbinder, Susan ^{[7
]}

Goedert, James J. ^{[4
]}

Winkler, Cheryl A. ^{[1
]}

机构：

[1] NCI, Lab Genom Div, SAIC Frederick, FCRDC, Frederick, MD 21702 USA

[2] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA

[3] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Mol Microbiol & Immunol, Baltimore, MD USA

[4] NCI, Infect & Immunoepidemiol Branch, Bethesda, MD 20892 USA

[5] Northwestern Univ, Chicago, IL 60611 USA

[6] Rho, Chapel Hill, NC USA

[7] San Francisco Dept Publ Hlth, San Francisco, CA USA

来源：

JOURNAL OF INFECTIOUS DISEASES | 2009年 / 200卷 / 07期

关键词：

VIF; STRATIFICATION; REPLICATION; INFECTION; GENE; AIDS;

D O I：

10.1086/605644

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

The human APOBEC3 family of cytidine deaminases provides intrinsic immunity to retroviral infection. A naturally occurring 29.5-kb deletion removes the entire APOBEC3B gene. We examined the impact of the APOBEC3B gene deletion in >4000 individuals from 5 human immunodeficiency virus type 1 (HIV-1) natural history cohorts. The hemizygous genotype had no effect on either acquisition of HIV-1 infection or progression to AIDS. However, the homozygous deletion was significantly associated with unfavorable outcomes for HIV-1 acquisition (odds ratio, 7.37; P = .024), progression to AIDS (relative hazard, 4.01; P = .03) and viral set point (P = .04). These findings suggest that the loss of APOPBEC3B may increase host susceptibility to HIV-1 acquisition and progression to AIDS and warrant further study.

引用

页码：1054 / 1058

页数：5

共 15 条

[1] APOBEC3G genetic variants and their influence on the progression to AIDS [J].