Association of DC-SIGN promoter polymorphism with increased risk for parenteral, but not mucosal, acquisition of human immunodeficiency virus type 1 infection
Association of DC-SIGN promoter polymorphism with increased risk for parenteral, but not mucosal, acquisition of human immunodeficiency virus type 1 infection
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DOI：
10.1128/jvi.78.24.14053-14056.2004
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发表时间：
2004-12-01
影响因子：
5.4
通讯作者：
Carrington, M
中科院分区：
文献类型：
--
作者：
Martin, MP;Lederman, MM;Carrington, M
关于人类免疫缺陷病毒1型（HIV-1）感染的基本机制和限制存在相当大的争论。鉴于最近的研究表明C型凝集素促进HIV-1感染的能力，我们根据感染途径探索了DC-SIGN启动子多态性与HIV-1感染风险之间的潜在关系。使用来自1,611名有肠外（n = 713）或粘膜（n = 898）感染风险的欧美参与者的样本，我们使用单链构象多态性鉴定了DC-SIGN启动子的单核苷酸多态性。有肠外获得性感染风险的-336C患者比-336T患者更容易感染（优势比= 1.87,P = 0.001）。在那些有粘膜获得性感染风险的人群中没有观察到这种关联。DC-SIGN对感染的系统性获取和传播具有潜在的特异性作用。
There is considerable debate about the fundamental mechanisms that underlie and restrict acquisition of human immunodeficiency virus type 1 (HIV-1) infection. In light of recent studies demonstrating the ability of C type lectins to facilitate infection with HIV-1, we explored the potential relationship between polymorphisms in the DC-SIGN promoter and risk for acquisition of HIV-1 according to route of infection. Using samples obtained from 1,611 European-American participants at risk for parenteral (n = 713) or mucosal (n = 898) infection, we identified single-nucleotide polymorphisms in the DC-SIGN promoter using single-strand conformation polymorphism. Individuals at risk for parenterally acquired infection who had -336C were more susceptible to infection than were persons with -336T (odds ratio = 1.87, P = 0.001). This association was not observed in those at risk for mucosally acquired infection. A potential role for DC-SIGN specific to systemic acquisition and dissemination of infection is suggested.