Department of Diagnostic Medicine and Pathobiology, College of Veterinary Medicine, Kansas State University, Manhattan, 1800 Denison Avenue, KS 66506, United States.
Department of Diagnostic Medicine and Pathobiology, College of Veterinary Medicine, Kansas State University, Manhattan, 1800 Denison Avenue, KS 66506, United States.
Virology. 2014 May;456-457:268-78. doi: 10.1016/j.virol.2014.04.002. Epub 2014 Apr 19.
Replication of porcine enteric calicivirus (PEC) in LLC-PK cells is dependent on the presence of bile acids in the medium. However, the mechanism of bile acid-dependent PEC replication is unknown. Understanding of bile acid-mediated PEC replication may provide insight into cultivating related human noroviruses, currently uncultivable, which are the major cause of viral gastroenteritis outbreaks in humans. Our results demonstrated that while uptake of PEC into the endosomes does not require bile acids, the presence of bile acids is critical for viral escape from the endosomes into cell cytoplasm to initiate viral replication. We also demonstrated that bile acid transporters including the sodium-taurocholate co-transporting polypeptide and the apical sodium-dependent bile acid transporter are important in exerting the effects of bile acids in PEC replication in cells. In summary, our results suggest that bile acids play a critical role in virus entry for successful replication.
猪肠道杯状病毒（PEC）在 LLC-PK 细胞中的复制依赖于培养基中胆汁酸的存在。然而，胆汁酸依赖型 PEC 复制的机制尚不清楚。了解胆汁酸介导的 PEC 复制可能有助于培养相关的人类诺如病毒，目前无法培养，这些病毒是人类病毒性胃肠炎爆发的主要原因。我们的研究结果表明，尽管 PEC 进入内体不需要胆汁酸，但胆汁酸的存在对于病毒从内体逃逸到细胞质中启动病毒复制至关重要。我们还表明，胆汁酸转运蛋白，包括牛磺胆酸钠共转运蛋白和顶端钠依赖性胆汁酸转运蛋白，在细胞中 PEC 复制中发挥胆汁酸的作用方面非常重要。总之，我们的结果表明胆汁酸在病毒进入以成功复制中发挥着关键作用。
