A new look at viruses in type 1 diabetes

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Article Abstract

Online ISSN: 1520-7560 Print ISSN: 1520-7552
Diabetes/Metabolism Research and Reviews
Volume 19, Issue 1, 2003. Pages: 8-31

Articles Available Online in Advance of Print
Published Online: 2 Dec 2002

Review Article

A new look at viruses in type 1 diabetes

Hee-Sook Jun, Dr Ji-Won Yoon^*

Julia McFarlane Diabetes Research Centre and Department of Microbiology and Infectious Diseases, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada

email: Ji-Won Yoon (yoon@ucalgary.ca)

^*Correspondence to Ji-Won Yoon, Julia McFarlane Diabetes Research Centre, Faculty of Medicine, University of Calgary, 3330 Hospital Drive N.W., Calgary, Alberta T2N, 4N1 Canada.

These two authors contributed equally

Keywords

virus • type 1 diabetes • environmental factor • virus-mediated autoimmunity • beta cell-specific autoimmunity

Abstract

Type 1 diabetes (T1D) results from the destruction of pancreatic beta cells. Genetic factors are believed to be a major component for the development of T1D, but the concordance rate for the development of diabetes in identical twins is only about 40%, suggesting that nongenetic factors play an important role in the expression of the disease. Viruses are one environmental factor that is implicated in the pathogenesis of T1D. To date, 14 different viruses have been reported to be associated with the development of T1D in humans and animal models. Viruses may be involved in the pathogenesis of T1D in at least two distinct ways: by inducing beta cell-specific autoimmunity, with or without infection of the beta cells, [e.g. Kilham rat virus (KRV)] and by cytolytic infection and destruction of the beta cells (e.g. encephalomyocarditis virus in mice). With respect to virus-mediated autoimmunity, retrovirus, reovirus, KRV, bovine viral diarrhoea-mucosal disease virus, mumps virus, rubella virus, cytomegalovirus and Epstein-Barr virus (EBV) are discussed. With respect to the destruction of beta cells by cytolytic infection, encephalomyocarditis virus, mengovirus and Coxsackie B viruses are discussed. In addition, a review of transgenic animal models for virus-induced autoimmune diabetes is included, particularly with regard to lymphocytic choriomeningitis virus, influenza viral proteins and the Epstein-Barr viral receptor. Finally, the prevention of autoimmune diabetes by infection of viruses such as lymphocytic choriomeningitis virus is discussed. Copyright © 2002 John Wiley & Sons, Ltd.

Received: 25 March 2002; Revised: 19 August 2002; Accepted: 27 August 2002

Digital Object Identifier (DOI)

10.1002/dmrr.337 About DOI

References are available in the Enhanced Abstract

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