Is type 1 diabetes "going viral"?

Abstract

Although genetic predisposition to type 1 diabetes (T1D) is a key risk factor, it does not explain the recent and rapid rise in incidence of the disease, particularly among children under the age of 5 (1). Changes in the environment and/or how individuals respond to these changes are now widely believed to be responsible for the recent increases in T1D. While viruses have been hypothesized to have an etiological role in T1D for more than five decades, definitive proof has not yet materialized. Nonetheless, a number of candidate viruses have been proposed, including enteroviruses, rotaviruses, herpesviruses, cytomegalovirus, and endogenous retroviruses (2). The strongest and most clinically significant associations point to enterovirus infection. A recent meta-analysis of 26 studies that assessed enteroviral infection using both molecular and immunological assays showed that compared with nondiabetic control subjects, the likelihood of finding evidence of enterovirus is 10-fold higher in T1D patients and fourfold higher in individuals with diabetes-related autoimmunity (3). Despite this evidence, important questions remain. These include whether a viral infection is causal in the development of T1D, whether it acts to accelerate the onset of disease in individuals in whom the process of β-cell destruction has already been initiated, or whether it is simply present because individuals with diabetes are more susceptible to infection. Two articles published in this issue of Diabetes help to address these questions. Ferreira et al. (4) and Kallionpaa et al. (5) used peripheral blood samples from two longitudinal birth cohorts—the BABYDIET cohort (6) and the Finnish Type 1 Diabetes Prediction and Prevention (DIPP) study (7), respectively. Both studies monitored development of diabetes-related autoantibodies as well as the onset of T1D in “at-risk” populations, thereby enabling access to samples …