Parker Alan L, McVey John H, Doctor Jessica H, Lopez-Franco Oscar, Waddington Simon N, Havenga Menzo J E, Nicklin Stuart A, Baker Andrew H
British Heart Foundation Glasgow Cardiovascular Research Centre, Division of Cardiovascular and Medical Sciences, University of Glasgow, 126 University Place, Glasgow G12 8TA, United Kingdom.
J Virol. 2007 Apr;81(7):3627-31. doi: 10.1128/JVI.02786-06. Epub 2007 Jan 24.
Recent evidence supports a role for vitamin K-dependent coagulation zymogens in adenovirus serotype 5 (Ad5, subgroup C) infection of hepatocytes. Here, we assessed the effect of virus-zymogen interaction on cellular transduction using a panel of fiber (f)-pseudotyped viruses derived from subgroup D (f47, f33, f24, f45, f17, f30). Each virus directly bound factor X (FX) as determined by surface plasmon resonance, resulting in enhanced cell surface binding. Infection of HepG2 cells was promoted by FX but not by FVII or FIX, while transduction of CHO cells was blocked in heparan sulfate proteoglycan-deficient cells. This suggests a broad role for FX in adenovirus infectivity.
最近的证据支持维生素K依赖的凝血酶原在腺病毒血清型5(Ad5,C亚组)感染肝细胞中发挥作用。在此,我们使用一组源自D亚组(f47、f33、f24、f45、f17、f30)的纤维(f)假型病毒评估了病毒-酶原相互作用对细胞转导的影响。通过表面等离子体共振测定,每种病毒都直接结合因子X(FX),导致细胞表面结合增强。FX促进了HepG2细胞的感染,但FVII或FIX则无此作用,而在硫酸乙酰肝素蛋白聚糖缺陷的细胞中,CHO细胞的转导受到了阻碍。这表明FX在腺病毒感染性中具有广泛作用。