Role of viruses in the pathogenesis of IDDM

Abstract

Insulin-dependent diabetes mellitus (IDDM), also known as type I diabetes, results from the destruction of pancreatic beta cells. During the past few decades, genetic factors, autoimmunity and viral infections have been extensively studied as the possible cause of beta cell destruction. The evidence for virus-induced diabetes comes largely from experiments in animals, but several studies in humans also point to viruses as a trigger of this disease in some cases. There are at least two possible mechanisms for the involvement of viruses in the pathogenesis of IDDM: (a) cytolytic infection of beta cells may result in destruction of the cells without the induction of autoimmunity, or may be a final insult leading to the clinical onset of diabetes in individuals with an already decreased beta cell mass resulting from an autoimmune process; and (b) persistent viral infection (e.g. retrovirus, rubella virus, cytomegalovirus) may result in the triggering of autoimmune IDDM in certain circumstances. Regarding the latter possibility, viruses may insert, expose, or alter antigens in the plasma membrane of the beta cell, which may initiate autoimmunity leading to the destruction of the cells.