Analysis of genetic polymorphisms in CCR5, CCR2, stromal cell-derived factor-1, RANTES, and dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin in seronegative individuals repeatedly exposed to HIV-1

被引：87
作者：
Liu, HL
Hwangbo, Y
Holte, S
Lee, J
Wang, CH
Kaupp, N
Zhu, HY
Celum, C
Corey, L
McElrath, MJ
Zhu, TF
机构：
[1] Univ Washington, Sch Med, Dept Lab Med, Seattle, WA 98195 USA
[2] Univ Washington, Sch Med, Dept Med, Seattle, WA 98195 USA
[3] Univ Washington, Sch Med, Dept Microbiol, Seattle, WA 98195 USA
[4] Fred Hutchinson Canc Res Ctr, Program Biostat, Seattle, WA 98104 USA
[5] Fred Hutchinson Canc Res Ctr, Program Infect Dis, Seattle, WA 98104 USA
来源：
JOURNAL OF INFECTIOUS DISEASES | 2004年 / 190卷 / 06期
关键词：
D O I：
10.1086/423209
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
To determine the influence of host genetics on human immunodeficiency virus (HIV) type 1 infection, we examined 94 repeatedly exposed seronegative (ES) individuals for polymorphisms in multiple genes and compared the results with those for 316 HIV-1-seropositive and 425 HIV-1-seronegative individuals. The frequency of homozygous C-C chemokine receptor (CCR) 5-Delta32 was higher in ES (3.2%) than in HIV-1-seropositive individuals (0.0%; P=.012). However, the CCR5-59029A, CCR2-64I, stromal cell-derived factor (SDF)-1-3'A, RANTES (regulated on activation, normally T cell-expressed and -secreted)-403A, and RANTES-28G polymorphisms were not associated with resistance to HIV-1 infection. Furthermore, we identified novel variants in the DC-SIGN (dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin) repeat region and observed that heterozygous DC-SIGN reduced the risk of HIV-1 infection (3.2% in ES individuals vs. 0.0% in HIV-1-seropositive individuals; P=.011).
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页码：1055 / 1058
页数：4
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