Association of DC-SIGN promoter polymorphism with increased risk for parenteral, but not mucosal, acquisition of human immunodeficiency virus type 1 infection

J Virol. 2004 Dec;78(24):14053-6. doi: 10.1128/JVI.78.24.14053-14056.2004.

Abstract

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.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Cell Adhesion Molecules / genetics*
  • Cohort Studies
  • HIV Infections / genetics*
  • HIV Infections / immunology
  • HIV Infections / physiopathology
  • HIV Infections / virology
  • HIV-1 / pathogenicity*
  • Humans
  • Infusions, Parenteral*
  • Lectins, C-Type / genetics*
  • Mucous Membrane
  • Polymorphism, Genetic*
  • Promoter Regions, Genetic / genetics*
  • Receptors, Cell Surface / genetics*

Substances

  • Cell Adhesion Molecules
  • DC-specific ICAM-3 grabbing nonintegrin
  • Lectins, C-Type
  • Receptors, Cell Surface