Cells infected with herpes simplex virus type 1 (HSV-1) express a cell-surface receptor able to bind the Fc portion of immunoglobulin G (IgG). In this study we provide direct evidence that bipolar bridging of antibodies, bound to the surface antigens on HSV-infected cells and to the Fc-receptor through the Fc part, offers the virus a survival advantage. Evidence was obtained by comparing the binding of FITC-labelled protein A, which has a similar binding site on IgG as the HSV-FcR, to cell-bound antibodies on HSV-infected cells and non-infected cells. The effectiveness of antibody bipolar bridging was dependent on the concentration of cell-bound IgG. At low concentrations of serum (0.1%) an 80% reduction in protein A-FITC binding to HSV-infected cells compared to non-infected cells was found. Even at higher concentrations of serum, antibody bipolar bridging resulted in a 40% reduction in the number of 'free' available Fc parts on HSV-infected cells compared to non-infected cells. Furthermore, these findings could be confirmed in a functional assay. The Fc-mediated attachment of granulocytes was significantly lower in HSV-infected cells compared to non-infected cells. From this study we conclude that HSV-FcR, by binding immune IgG in a bipolar fashion, provides the virus with an effective defence mechanism.