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Adv Dent Res 19:42-48, April, 2006
© 2006 International and American Associations for Dental Research

Role of Human ß-defensins in HIV Infection

Presented at the Fifth World Workshop on Oral Health and Disease in AIDS, Phuket, Thailand, July 6–9, 2004, sponsored by Prince of Songkla University, Thailand, the International Association for Dental Research, the World Health Organization, the NIDCR/National Institutes of Health, USA, and the University of California-San Francisco Oral AIDS Center.

A. Weinberg1,*, M.E. Quiñones-Mateu2, and M.M. Lederman3

1 Department of Biological Sciences, School of Dental Medicine, Case Western Reserve University (CWRU), 10900 Euclid Ave., Cleveland, OH 44106, USA
2 Lerner Research Institute, Cleveland Clinic Foundation, Center for AIDS Research, CWRU; and
3 University Hospitals of Cleveland, OH

Correspondence: * corresponding author, aaron.weinberg{at}case.edu.

Mechanisms of resistance to HIV-1 infection in the human oral cavity are incompletely understood. While salivary components have been implicated in protection, there is growing evidence that human beta-defensins (hBDs), originating in oral epithelial cells, may be playing an important role in the prevention of HIV infection. New antiviral, chemotactic, and immunosurveillance properties are being attributed to hBDs, which are small cationic antimicrobial innate response molecules expressed in mucosal epithelium. Inducible hBDs are always expressed in normal oral epithelium, a property not shared by other mucosal barriers. Data reviewed in this paper demonstrate that: (1) HIV-1 X4 and R5 phenotypes induce hBD-2 and -3 mRNA in normal human oral epithelial cells; (2) hBD-2 and -3 inhibit HIV-1 infection by both viral strains, with greater activity against X4 viruses; and (3) this inhibition is due to a direct interaction with virions and through modulation of the CXCR4 co-receptor. These properties may be exploited as strategies for mucosal protection against HIV-1 transmission.

KEY WORDS: Human beta-defensin • epithelial cell • innate immunity • HIV




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