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Quiñones-Mateu, M.E. et al.

Human epithelial beta-defensins 2 and 3 inhibit HIV-1 replication.

OBJECTIVE: Mechanisms underlying mucosal transmission of HIV-1 are incompletely understood. We describe the anti-HIV-1 activity of human beta-defensins (hBD), small cationic molecules that provide protection at mucosal surfaces. METHODS AND RESULTS: HIV-1 induced expression of hBD-2 and -3 mRNA (but not that of hBD-1) 4- to 78-fold, respectively, above baseline in normal human oral epithelial cells. HIV-1 failed to infect these cells, even after 5 days of exposure. Recombinant hBD-1 had no antiviral activity, while rhBD-2 and rhBD-3 showed concentration-dependent inhibition of HIV-1 replication without cellular toxicity. Inhibition was greater against CXCR4-tropic than against the CCR5-tropic HIV-1 isolates. hBD-2 and hBD-3 induced an irreversible effect on virion infectivity, with electron microscopy confirming binding of hBDs to viral particles. Finally, hBD-2 and -3 induced downmodulation of the HIV-1 coreceptor CXCR4 (but not CCR5) in peripheral blood mononuclear cells and T lymphocytic cells as shown by confocal microscopy and flow cytometry. CONCLUSIONS: This study shows for the first time that HIV-1 induces beta-defensin expression in human oral epithelial cells and that beta-defensins block HIV-1 replication via a direct interaction with virions and through modulation of the CXCR4 coreceptor. These properties may be exploited as strategies for mucosal protection against HIV-1 transmission.[1]

References

Human epithelial beta-defensins 2 and 3 inhibit HIV-1 replication. Quiñones-Mateu, M.E., Lederman, M.M., Feng, Z., Chakraborty, B., Weber, J., Rangel, H.R., Marotta, M.L., Mirza, M., Jiang, B., Kiser, P., Medvik, K., Sieg, S.F., Weinberg, A. AIDS (2003) [Pubmed]

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