| Summary: | <p>Abstract</p> <p>Background</p> <p>HIV-1 in genital secretions may be opsonized by several molecules including complement components. Opsonized HIV-1 by complement enhances the infection of various mucosal target cells, such as dendritic cells (DC) and epithelial cells.</p> <p>Results</p> <p>We herein evaluated the effect of HIV-1 complement opsonization on microbicide candidates' activity, by using three <it>in vitro </it>mucosal models: CCR5-tropic HIV-1<sub>JR-CSF </sub>transcytosis through epithelial cells, HIV-1<sub>JR-CSF </sub>attachment on immature monocyte-derived dendritic cells (iMDDC), and infectivity of iMDDC by CCR5-tropic HIV-1<sub>BaL </sub>and CXCR4-tropic HIV-1<sub>NDK</sub>. A panel of 10 microbicide candidates [T20, CADA, lectines HHA & GNA, PVAS, human lactoferrin, and monoclonal antibodies IgG1B12, 12G5, 2G12 and 2F5], were investigated using cell-free unopsonized or opsonized HIV-1 by complements. Only HHA and PVAS were able to inhibit HIV trancytosis. Upon opsonization, transcytosis was affected only by HHA, HIV-1 adsorption on iMDDC by four molecules (lactoferrin, IgG1B12, IgG2G5, IgG2G12), and replication in iMDDC of HIV-1<sub>BaL </sub>by five molecules (lactoferrin, CADA, T20, IgG1B12, IgG2F5) and of HIV-1<sub>NDK </sub>by two molecules (lactoferrin, IgG12G5).</p> <p>Conclusion</p> <p>These observations demonstrate that HIV-1 opsonization by complements may modulate <it>in vitro </it>the efficiency of candidate microbicides to inhibit HIV-1 infection of mucosal target cells, as well as its crossing through mucosa.</p>
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