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Animal: RNA Viruses |
Department of Molecular Pathology, Institute for Pathology, University of Tübingen, Liebermeisterstr. 8, D-72076 Tübingen, Germany1
Author for correspondence: Hans-Christoph Selinka. Fax +49 7071 29 5334. e-mail hans-christoph.selinka{at}med.uni-tuebingen.de
Decay-accelerating factor (DAF/CD55), and coxsackievirus–adenovirus receptor (CAR) have been identified as cellular receptors for coxsackie B viruses (CBV). To elucidate the interplay of DAF and CAR on the cell surface, virus–receptor interactions of two coxsackieviruses of serotype B3 (non-haemagglutinating CBV3 and haemagglutinating CBV3-HA strain) were analysed. Binding assays revealed clear differences between these viruses with regard to their interactions with DAF and CAR. However, only the combination of anti-DAF and anti-CAR antibodies resulted in complete inhibition of virus binding for both strains. In plaque-reduction assays, anti-DAF antibodies had no effect, whereas CAR-specific antibodies significantly reduced productive infection of HeLa cells by both viruses. Interestingly, a synergistic inhibitory effect of anti-DAF and anti-CAR antibodies was also observed with regard to infection. These findings support the model of preferential interactions of both strains of CBV3 with closely associated DAF and CAR proteins on HeLa cells, despite displaying clear differences in their binding phenotypes.
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