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CUTTING EDGE |
* Department of Hygiene, Microbiology and Social Medicine, Innsbruck Medical University and Ludwig-Boltzman-Institute for AIDS Research, Innsbruck, Austria; and
Department of Immunology and Research Group of the Hungarian Academy of Sciences, Eötvös Loránd University, Budapest, Hungary
In the present study, we demonstrate that macrophage-tropic HIV-1 opsonized by complement and limited amounts of anti-HIV-IgG causes up to 10-fold higher productive infection of human monocyte-derived dendritic cells than HIV treated with medium or HIV opsonized by Ab only. Enhanced infection is completely abolished by a mAb specific for the ligand-binding site of CD11b (i.e., 
-chain of complement receptor 3, receptor for iC3b), proving the importance of complement receptor 3 in this process. Inhibition of complement activation by EDTA also prevents enhanced infection, further demonstrating the role of complement in virus uptake and productive infection. Since HIV is, even in the absence of Abs, regularly opsonized by complement, most probably the above-described mechanism plays a role during in vivo primary infection.
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