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A Silver Nanoparticle Method for Ameliorating Biliary Atresia Syndrome in Mice
Published on: October 13, 2018
Effect of rotavirus strain on the murine model of biliary atresia
Steven R Allen1, Mubeen Jafri, Bryan Donnelly
1Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue, MLC 2923, Cincinnati, OH 45229, USA.
Insights
Rotavirus strain tropism determines biliary epithelial cell infection, impacting biliary atresia development in a mouse model. Specific strains cause disease, while others do not, highlighting strain-specific characteristics.
Area of Science:
- Virology
- Hepatology
- Neonatal Disease
Background:
- Biliary atresia is a severe neonatal liver disease causing inflammation and fibrosis of the extrahepatic biliary tract.
- Viral infection is a suspected contributing factor to the etiology of biliary atresia.
- Rhesus rotavirus (RRV) in a murine model causes biliary epithelial cell infection, leading to bile duct obstruction.
Purpose of the Study:
- To investigate if tropism for biliary epithelial cells is unique to RRV.
- To evaluate the impact of different rotavirus strains on the murine model of biliary atresia.
Main Methods:
- Newborn mice were intraperitoneally injected with five rotavirus strains: RRV, SA11-FM, SA11-SM, EDIM, and Wa.
- Clinical manifestations, mortality, and viral distribution were assessed.
- Immunohistochemistry was used to determine viral tropism for biliary epithelial cells.
Main Results:
- RRV and SA11-FM induced bile duct obstruction and high mortality.
- SA11-SM caused hepatobiliary injury with reduced mortality.
- EDIM and Wa did not cause hepatobiliary disease; RRV and SA11-FM targeted biliary epithelial cells, while SA11-SM did not.
Conclusions:
- Rotavirus strain-specific characteristics dictate tropism for hepatobiliary cells.
- Tropism for biliary epithelial cells is crucial for inducing the murine model of biliary atresia.
- Understanding strain-specific tropism is key to modeling biliary atresia.
Abstract:
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.
