@article{770908535de64c438212b49b76a3923e,
title = "APOBEC3B deletion and risk of HIV-1 acquisition",
abstract = "The human AFOBEC3 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 APOBEC3B may increase host susceptibility to HIV-1 acquisition and progression to AIDS and warrant further study.",
author = "Ping An and Randall Johnson and John Phair and Kirk, {Gregory D.} and Yu, {Xiao Fang} and Sharyne Donfield and Susan Buchbinder and Goedert, {James J.} and Winkler, {Cheryl A.}",
note = "Funding Information: Received 9 February 2009; accepted 29 April 2009; electronically published 21 August 2009. Potential conflicts of interest: none reported. Financial support: Intramural Research Program, Center for Cancer Research, National Cancer Institute (grants HHSN261200800001E and N02-CP-55504); National Institute on Drug Abuse (grants R01-DA04334 and R01-12586). Presented in part: 59th Annual Meeting of the American Society of Human Genetics, Philadelphia, PA, 11–15 November 2008 (abstract 2196). The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the US government. Reprints or correspondence: Dr Cheryl Winkler, NCI-FCRDC, Bldg 560, Frederick, MD 21702 (winkler@ncifcrf.gov).",
year = "2009",
month = oct,
day = "1",
doi = "10.1086/605644",
language = "English (US)",
volume = "200",
pages = "1054--1058",
journal = "Journal of Infectious Diseases",
issn = "0022-1899",
publisher = "Oxford University Press",
number = "7",
}