Abstract
Coxsackieviruses B (CV-B) belong to the EV-B species. CV-B and particularly CV-B4 are thought to be involved in the development of chronic diseases like type 1 diabetes (T1D). The mechanisms of the enteroviral pathogenesis of T1D are not well known, yet. The in vitro studies are rich with information but in vivo infection models are needed to investigate the impact of viruses onto organs. Our objective was to study the impact of CV-B4E2 combined with a single sub-diabetogenic dose of streptozotocin (STZ) on the pancreas of mice. The infection with CV-B4E2 of CD1 outbred mice treated with a sub-diabetogenic dose of STZ induced hyperglycemia and hypoinsulinemia. Along with the chemokine IP-10, viral RNA and infectious particles were detected in the pancreas. The pancreas of these animals was also marked with insulitis and other histological alterations. The model combining STZ and CV-B4E2 opens the door to new perspectives to better understand the interactions between virus and host, and the role of environmental factors capable, like STZ, to predispose the host to the diabetogenic effects of enteroviruses.
Highlights
Coxsackievirus B (CVB) 1 to 6, are viruses with RNA genome that belong to the species Enterovirus B (EV-B), of the Enterovirus genus of the Picornaviridae family
Diabetes induced by CV-B4E2 in mice treated with a sub-diabetogenic dose of streptozotocin
Blood glucose levels in control mice injected with culture medium, CV-B4E2, or a sub-diabetogenic dose of STZ were lower than 300 mg/dl (300 mg/dL is the threshold for hyperglycemia) whereas they were higher in animals treated with STZ combined with CV-B4E2
Summary
Coxsackievirus B (CVB) 1 to 6, are viruses with RNA genome that belong to the species Enterovirus B (EV-B), of the Enterovirus genus of the Picornaviridae family. Diabetes can be induced by streptozotocin (STZ), a glucosamine-nitrosourea compound that targets pancreatic β cells. It was isolated for the first time from the Streptomyces achromogenes bacteria. Insulin-producing cells that do not express GLUT2 are resistant to STZ toxicity[19]. Once inside, it is rapidly metabolized and affects the DNA and the mitochondria. The purpose of the present study was to investigate the impact of CV-B4E2 combined with a single sub-diabetogenic dose of streptozotocin on the pancreas and on pancreatic β cells of outbred mice
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