Coxsackievirus B3-induced acute pancreatitis: analysis of histopathological and viral parameters in a mouse model.

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.