Viral diabetes mellitus in man and experimental animals.

Accumulating evidence strongly suggests that viruses may play an etiologic role in some cases of diabetes mellitus. The importance of environmental factors in the pathogenesis of the disease is suggested by genetic and epidemiological observations. Group B Coxsackie viruses and mumps virus have been implicated, and the evidence suggests that several other agents also could play a role in the disease. In experimental animals, a picornavirus similar to the Coxsackie viruses exhibits specific tropism for the beta cells of the islets of Langerhans, causing a disease in mice that is similar to juvenile-onset diabetes. In these animals, genetic and metabolic factors appear to influence the severity of beta cell injury. Immunopathologic considerations also may be important. In man, histocompatibility genes are important determinants of juvenile-onset diabetes and abberations of immune responsiveness to beta cells have been demonstrated. In experimental animals, cell-mediated immunity develops subsequent to the occurrence of viral-induced lesions in the islets. Viewed in concert, the evidence supports the notion that certain "wild" viruses may possess specific tropism for beta cells and destroy them during the course of a systemic infection. Host factors clearly play a role, but their relative importance in the pathogenesis of the disease remains to be defined.