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Journal of Virology, December 2004, p. 14053-14056, Vol. 78, No. 24
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.24.14053-14056.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

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

Maureen P. Martin,1 Michael M. Lederman,2 Holli B. Hutcheson,3 James J. Goedert,4 George W. Nelson,1 Yvette van Kooyk,5 Roger Detels,6 Susan Buchbinder,7 Keith Hoots,8 David Vlahov,9 Stephen J. O'Brien,3 and Mary Carrington1*

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.

* Corresponding author. Present address: SAIC-Frederick, National Cancer Institute, P.O. Box B, Frederick, MD 21702. Phone: (301) 846-1390. Fax: (301) 846-6771. E-mail: carringt{at}ncifcrf.gov.

Journal of Virology, December 2004, p. 14053-14056, Vol. 78, No. 24
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.24.14053-14056.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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