Differential activity of candidate microbicides against early steps of HIV-1 infection upon complement virus opsonization

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• 作者：Mohammad-Ali Jenabian (1)
  Héla Sa?di (1)
  Charlotte Charpentier (1)
  Hicham Bouhlal (2)
  Dominique Schols (3)
  Jan Balzarini (3)
  Thomas W Bell (4)
  Guido Vanham (5)
  Laurent Bélec (1)
  
• 刊名：AIDS Research and Therapy
• 出版年：2010
• 出版时间：December 2010
• 年：2010
• 卷：7
• 期：1
• 全文大小：601KB
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• 作者单位：Mohammad-Ali Jenabian (1)
  Héla Sa?di (1)
  Charlotte Charpentier (1)
  Hicham Bouhlal (2)
  Dominique Schols (3)
  Jan Balzarini (3)
  Thomas W Bell (4)
  Guido Vanham (5)
  Laurent Bélec (1)
  
  1. Laboratoire de Virologie, H?pital Européen Georges Pompidou, Université Paris Descartes (Paris V), Paris, France
  2. Inserm U925, Laboratoire d'Immunologie, faculté de Médecine, Université Jules Verne Picardie, Amiens, France
  3. Rega Institute for Medical Research, Leuven, Belgium
  4. University of Nevada, Reno, NV, USA
  5. Virology Unit, Department of Microbiology, Institute of Tropical Medicine, Antwerpen, Belgium
  
• ISSN：1742-6405

文摘

Background 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. Results We herein evaluated the effect of HIV-1 complement opsonization on microbicide candidates' activity, by using three in vitro mucosal models: CCR5-tropic HIV-1JR-CSF transcytosis through epithelial cells, HIV-1JR-CSF attachment on immature monocyte-derived dendritic cells (iMDDC), and infectivity of iMDDC by CCR5-tropic HIV-1BaL and CXCR4-tropic HIV-1NDK. 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-1BaL by five molecules (lactoferrin, CADA, T20, IgG1B12, IgG2F5) and of HIV-1NDK by two molecules (lactoferrin, IgG12G5). Conclusion These observations demonstrate that HIV-1 opsonization by complements may modulate in vitro the efficiency of candidate microbicides to inhibit HIV-1 infection of mucosal target cells, as well as its crossing through mucosa.