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Association of DC-SIGN Promoter Polymorphism with Increased Risk for Parenteral, but Not Mucosal, Acquisition of Human Immunodeficiency Virus Type 1 Infection

Basic Research Program, SAIC Frederick,¹ Laboratory of Genomic Diversity, National Cancer Institute, Frederick,³ Viral Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland,⁴ Center for AIDS Research, University Hospitals, Case Western Reserve University, Cleveland, Ohio,² Department of Molecular Cell Biology, Vrije Universiteit Medical Center, Amsterdam, The Netherlands,⁵ Department of Epidemiology, School of Public Health, University of California, Los Angeles, Los Angeles,⁶ San Francisco Department of Public Health, San Francisco, California,⁷ Gulf States Hemophilia Center, University of Texas Health Science Center, Houston, Texas,⁸ Center for Urban Epidemiologic Studies, New York Academy of Medicine, New York, New York⁹

Received 4 May 2004/ Accepted 27 July 2004

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.

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