A new look at viruses in type 1 diabetes

Type 1 diabetes results from the destruction of pancreatic beta cells. Genetic factors are believed to be a major component for the development of type 1 diabetes, but the concordance rate for the development of diabetes in identical twins is only about 40%, suggesting that non-genetic factors play an important role in the expression of the disease. Viruses are one environmental factor that is implicated in the pathogenesis of type 1 diabetes. To date, 14 different viruses have been reported to be associated with the development of type 1 diabetes in humans and animal models. Viruses may be involved in the pathogenesis of type 1 diabetes 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) and by cytolytic infection and destruction of the beta cells (e.g. encephalomyocarditis virus in mice). With respect to virus-mediated autoimmunity, retrovirus, reovirus, Kilham rat virus, bovine viral diarrhoea-mucosal disease virus, mumps virus, rubella virus, cytomegalovirus and Epstein-Barr virus 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.