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Factor I-Mediated Processing of Complement Fragments on HIV Immune Complexes Targets HIV to CR2-Expressing B Cells and Facilitates B Cell-Mediated Transmission of Opsonized HIV to T Cells¹

Zoltán Bánki^2,*, Doris Wilflingseder^*, Christoph G. Ammann^*, Monika Pruenster^*, Brigitte Müllauer^*, Karoline Holländer, Martina Meyer, Georg M. Sprinzl, Jan van Lunzen, Hans-Jürgen Stellbrink, Manfred P. Dierich^* and Heribert Stoiber^*

^* Department of Hygiene, Microbiology and Social Medicine, Innsbruck Medical University; and Ludwig Boltzmann Institute for AIDS Research, Innsbruck, Austria; Department of Medicine, Eppendorf University, Hamburg, Germany; and Central Institute for Blood Transfusion and Division for Immunology and Department of Otorhinolaryngology, University Hospital, Innsbruck, Austria

Our study demonstrates that binding of complement-opsonized HIV to complement receptor type 1 on human erythrocytes (E) via C3b fragments is followed by a rapid normal human serum-mediated detachment of HIV from E. The release was dependent on the presence of factor I indicating a conversion of C3b fragments to iC3b and C3d on the viral surface. This in turn resulted in an efficient binding of opsonized HIV to CR2-expressing B cells, thus facilitating B cell-mediated transmission of HIV to T cells. These data provide a new dynamic view of complement opsonization of HIV, suggesting that association of virus with E might be a transient phenomenon and the factor I-mediated processing of C3b to iC3b and C3d on HIV targets the virus to complement receptor type 2-expressing cells. Thus, factor I in concert with CR1 on E and factor H in serum due to their cofactor activity are likely to be important contributors for the generation of C3d-opsonized infectious HIV reservoirs on follicular dendritic cells and/or B cells in HIV-infected individuals.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by Grants P14661 (to M.P.D.) and P17914 (to H.S.) from the Fonds zur Förderung der Wissenschaftlichen Forschung, Grants QLK-CT-2002-00882 (to H.S.), and TIP/VAC-012116 (to H.S.) from the 5th and 6th framework of the European Union, grants from the Ludwig-Boltzmann-Institute for AIDS Research, grants from the German Federal Ministry of Research (to H-J. S., Competence Network HIV, 01KI0211), and grants from the Government of Tyrol.

² Address correspondence and reprint requests to Dr. Zoltán Bánki, Department of Hygiene, Microbiology and Social Medicine, Innsbruck Medical University, Fritz-Pregl-Strasse 3, 6020 Innsbruck, Austria. E-mail address: Zolta.Banki{at}uibk.ac.at

³ Abbreviations used in this paper: FDC, follicular dendritic cell; CR, complement receptor; IC, immune complex; fI, factor I; NHS, normal human serum; hiNHS, heat-inactivated NHS; AEBSF, 4-(2-aminoethyl)-benzenesulfonyl fluoride; fH, factor H; w/o, without; DC dendritic cell; E, erythrocyte.