Format

Send to

Choose Destination
Virology. 2014 May;456-457:268-78. doi: 10.1016/j.virol.2014.04.002. Epub 2014 Apr 19.

The crucial role of bile acids in the entry of porcine enteric calicivirus.

Author information

1
Department of Diagnostic Medicine and Pathobiology, College of Veterinary Medicine, Kansas State University, Manhattan, 1800 Denison Avenue, KS 66506, United States.
2
Department of Diagnostic Medicine and Pathobiology, College of Veterinary Medicine, Kansas State University, Manhattan, 1800 Denison Avenue, KS 66506, United States. Electronic address: kchang@vet.ksu.edu.

Abstract

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.

KEYWORDS:

Bile acids; Bile transporters; Endosomal escape; Porcine enteric calicivirus; Virus entry

PMID:
24889246
PMCID:
PMC4064365
DOI:
10.1016/j.virol.2014.04.002
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center