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Journal of Virology, February 2007, p. 1671-1679, Vol. 81, No. 4
0022-538X/07/$08.00+0     doi:10.1128/JVI.02094-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Effect of Rotavirus Strain on the Murine Model of Biliary Atresia{triangledown}

Steven R. Allen,1 Mubeen Jafri,1 Bryan Donnelly,1 Monica McNeal,2 David Witte,3 Jorge Bezerra,4 Richard Ward,2 and Gregory M. Tiao1*

The Department of Pediatric Surgery,1 The Division of Infectious Disease,2 The Department of Pathology,3 The Division of Gastroenterology, Hepatology, and Nutrition, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio4

Received 25 September 2006/ Accepted 10 November 2006

Biliary atresia is a devastating disorder of the newborn in which afflicted infants develop inflammation and fibrosis of the extrahepatic biliary tract, resulting in cirrhosis and end-stage liver disease. Infection with a virus is thought to be a contributing factor in the etiology of biliary atresia. In the murine model of biliary atresia, perinatal exposure to rhesus rotavirus (RRV) results in biliary epithelial cell infection causing bile duct obstruction. The purpose of this study was to determine if tropism for the biliary epithelial cell was unique to RRV. Newborn mice underwent intraperitoneal injection with five strains of rotavirus: RRV (simian), SA11-FM (simian/bovine), SA11-SM (simian), EDIM (murine), and Wa (human). RRV and SA11-FM caused clinical manifestations of bile duct obstruction and high mortality. SA11-SM caused clinical signs of hepatobiliary injury but the mortality was markedly reduced. EDIM and Wa caused no sign of hepatobiliary disease. The systemic and temporal distribution of viral protein and live virus varied according to the injected strain. Immunohistochemistry revealed that RRV and SA11-FM targeted the biliary epithelial cells. In contrast, SA11-SM was found in the liver but in not in the biliary epithelium. These results indicate that strain-specific characteristics dictate tropism for cells of hepatobiliary origin which in turn impact the ability to induce the murine model of biliary atresia.

* Corresponding author. Mailing address: Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue, MLC 2923, Cincinnati, OH 45229. Phone: (513) 636-2292. Fax: (513) 636-7657. E-mail: greg.tiao{at}cchmc.org.

{triangledown} Published ahead of print on 22 November 2006.

Journal of Virology, February 2007, p. 1671-1679, Vol. 81, No. 4
0022-538X/07/$08.00+0     doi:10.1128/JVI.02094-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Feng, N., Kim, B., Fenaux, M., Nguyen, H., Vo, P., Omary, M. B., Greenberg, H. B. (2008). Role of Interferon in Homologous and Heterologous Rotavirus Infection in the Intestines and Extraintestinal Organs of Suckling Mice. J. Virol. 82: 7578-7590 [Abstract] [Full Text]  
  • Jafri, M., Donnelly, B., Allen, S., Bondoc, A., McNeal, M., Rennert, P. D., Weinreb, P. H., Ward, R., Tiao, G. (2008). Cholangiocyte expression of {alpha}2{beta}1-integrin confers susceptibility to rotavirus-induced experimental biliary atresia. Am. J. Physiol. Gastrointest. Liver Physiol. 295: G16-G26 [Abstract] [Full Text]  


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