The case for virus-induced type 1 diabetes.

PURPOSE OF REVIEW

Type 1 diabetes (T1D) results from the immune-mediated destruction of pancreatic insulin-producing cells because of the interaction among genetic susceptibility, the immune system and environmental factor(s). A possible role of viral infections in T1D pathogenesis has been hypothesized for some time; however, only in the most recent years, studies performed at the molecular and cellular level are starting to shed light on this issue.

RECENT FINDINGS

Studies in animal models and in man have shown that viruses can indeed infect pancreatic beta-cells, inducing islet inflammation and functional damage. In addition, recent in-situ investigations performed on pancreatic tissue samples have provided evidence that in addition to adaptive immune response, innate immunity is involved in T1D pathogenesis and the whole pancreas (not only its endocrine portion) is infiltrated by immune-mediated phenomena.

SUMMARY

The established role of inflammation in the insulitic process and the increasing evidence in support of the contribution of viral infections to a proinflammatory islet scenario are strongly suggestive that viruses may indeed contribute to beta-cell damage and dysfunction, thus setting the stage for the design of antiviral strategies (e.g. vaccines and antiviral drugs) aimed at protecting the beta-cells.