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Coxsackievirus B3-induced acute pancreatitis: analysis of histopathological and viral parameters in a mouse model
T Vuorinen1, M Kallajoki, T Hyypiä
1Department of Virology, University of Turku, Finland.
Abstract:
Coxsackievirus B3 infection in mice was studied histopathologically, by virus isolation and by nucleic acid hybridization after intraperitoneal inoculation of the virus. Extensive viraemia was detected for 1-3 days post-infection. All mice developed necrotizing acute pancreatitis and focal myocarditis. Pancreatitis eventually lead to complete atrophy of the exocrine pancreas. However, the islets of Langerhans and pancreatic ducts remained morphologically intact. Virus could be demonstrated in pancreatic tissue for 1-5 days post-infection by in-situ and spot hybridization as well as by virus isolation. Virus was not detectable on days 7-22 post-infection suggesting an autodigestive aetiology in further destruction of the exocrine pancreas. The mouse model described here permits detailed analysis of viral and host factors in the pathogenesis of enterovirus infections. Since coxsackie B viruses have been proposed to be aetiological agents in human acute pancreatitis, the application of in-situ hybridization allows analysis of enteroviruses directly from pancreatic tissue of clinical routine specimens.
Insights
Coxsackievirus B3 causes acute pancreatitis and myocarditis in mice, leading to exocrine pancreas atrophy. This mouse model aids enterovirus infection research and analyzing clinical pancreatitis samples.
Area of Science:
- Virology
- Pathology
- Immunology
Background:
- Enteroviruses, including Coxsackievirus B3 (CVB3), are implicated in human acute pancreatitis.
- Understanding the viral and host factors in enterovirus-induced pancreatitis is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the histopathological effects and viral dynamics of Coxsackievirus B3 infection in a mouse model.
- To establish a reliable mouse model for studying enterovirus-induced pancreatitis and its pathogenesis.
Main Methods:
- Intraperitoneal inoculation of CVB3 in mice.
- Histopathological examination of infected tissues.
- Virus isolation and nucleic acid hybridization (in-situ and spot hybridization) for viral detection.
Main Results:
- Widespread viremia occurred within 1-3 days post-infection.
- All infected mice developed necrotizing acute pancreatitis and focal myocarditis.
- Pancreatitis led to exocrine pancreas atrophy, while islets and ducts remained intact. Virus was detected in pancreatic tissue for 1-5 days, with subsequent clearance suggesting autodigestion in further pancreatic destruction.
- Virus was not detectable on days 7-22 post-infection.
Conclusions:
- The described mouse model effectively replicates key features of CVB3-induced pancreatitis and myocarditis.
- The findings suggest an autodigestive mechanism contributes to pancreatic damage following viral clearance.
- This model is valuable for analyzing viral and host factors in enterovirus pathogenesis and offers potential for direct enterovirus analysis in human clinical samples using in-situ hybridization.