Pasch Andreas, Küpper Jan-Heiner, Wolde Antje, Kandolf Reinhard, Selinka Hans-Christoph
Department of Molecular Pathology, Institute for Pathology, University of Tübingen, Liebermeisterstr. 8, D-72076 Tübingen, Germany1.
J Gen Virol. 1999 Dec;80 ( Pt 12):3153-3158. doi: 10.1099/0022-1317-80-12-3153.
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.
衰变加速因子(DAF/CD55)和柯萨奇病毒-腺病毒受体(CAR)已被确定为柯萨奇B组病毒(CBV)的细胞受体。为了阐明DAF和CAR在细胞表面的相互作用,分析了两种B3血清型柯萨奇病毒(非血凝性CBV3和血凝性CBV3-HA株)的病毒-受体相互作用。结合试验揭示了这些病毒在与DAF和CAR相互作用方面的明显差异。然而,只有抗DAF和抗CAR抗体的组合才能完全抑制两种毒株的病毒结合。在蚀斑减少试验中,抗DAF抗体没有作用,而CAR特异性抗体显著降低了两种病毒对HeLa细胞的有效感染。有趣的是,在感染方面也观察到抗DAF和抗CAR抗体的协同抑制作用。这些发现支持了CBV3两种毒株与HeLa细胞上紧密相关的DAF和CAR蛋白优先相互作用的模型,尽管它们的结合表型存在明显差异。