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Sci Rep. 2019 Jul 12;9(1):10080. doi: 10.1038/s41598-019-46227-3.

Impact of coxsackievirus-B4E2 combined with a single low dose of streptozotocin on pancreas of outbred mice: investigation of viral load, pathology and inflammation.

Author information

1
Université de Lille, Faculté de Médecine, CHU de Lille, Laboratoire de Virologie/EA3610, F-59037, Lille, France.
2
Université de Monastir, Faculté de Pharmacie, Laboratoire des Maladies Transmissibles et Substances Biologiquement Actives LR99ES27, Monastir, Tunisia.
3
Université de Tunis El Manar, Faculté des Sciences de Tunis, Tunis, Tunisia.
4
Université de Picardie Jules Verne, CHU d'Amiens, Service d'Endocrinologie-Diabétologie-Nutrition, F-80054, Amiens, France.
5
Université de Lille, Faculté de Médecine, CHU de Lille, Laboratoire de Virologie/EA3610, F-59037, Lille, France. didier.hober@chru-lille.fr.

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.

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