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Despite a large number of epidemiologic associations, clinical studies, and animal models, a direct involvement of pathogens in the etiology of human type 1 diabetes is still a matter of critical debate. Human enteroviruses (HEV), such as coxsackievirus B (CVB) and echoviruses (EV), have been associated with type 1 diabetes since the late 1960s (1) and have been found in pancreatic isolates of type 1 diabetic patients (2–4) (rev. in 5). However, there are several difficulties hampering the conviction of HEV as inducers of type 1 diabetes: 1 ) pancreatic biopsies are not done on a regular basis in type 1 diabetic patients; 2 ) HEV infections are frequently found in nondiabetic individuals and often remain asymptomatic; 3 ) the clinical manifestation of type 1 diabetes may occur years to decades after infection (virus infection as a “hit-and-run” event); 4 ) type 1 diabetic patients as well as healthy individuals undergo multiple virus infections throughout their lifetime, some of which might even protect them from rather than induce autoimmune disease; and 5 ) genetic predispositions might cover possible environmental (i.e., virus) factors.In this issue of Diabetes , Schulte et al. (6) address the mechanism by which HEV infection of human islets might influence type 1 diabetes onset and/or progression. They found that monocyte-derived dendritic cells (DCs) efficiently phagocytosed CVB3-infected human and porcine islets. Phagocytosis of CVB3-infected islets induced the …

Enterovirus Infection of Human β-Cells Activates Dendritic Cells and Triggers Innate Antiviral Responses: Are Enteroviruses Convicted Now?