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As if the pathway of regulation leading islet cells toward dysfunction and diabetes was not difficult enough to grasp, here come viruses to further complicate matters. In the past few years, we have come to recognize that a class of small noncoding RNAs termed microRNAs (miRNAs) has a powerful ability to regulate most, if not all, of the key processes in cell biology (1,2). In fact, there is evidence that these key molecules can be transported from cell to cell, thereby influencing gene expression not only within the host cell but also in neighboring cells and in distant cell subsets when the miRNAs travel in vesicles via the blood and lymph (3–5).The evidence that miRNAs play pivotal roles in β-cell biology, including regulating their differentiation, glucose responsiveness, insulin production, apoptosis, and inflammation, is rapidly accumulating and was recently discussed by Filios and Shalev (4) in an issue of Diabetes . As one might expect given their range of functions within the β-cells, these same molecules are hypothesized to have key roles in the pathogenesis of type 1 diabetes (4,6–13). Yet, it is still not clear whether or not they are central to the induction of disease or if they are merely a biomarker of active β-cell dysfunction.Type 1 diabetes is often described as a chronic autoimmune disease characterized by the destruction of insulin-producing islet β-cells, and it is a widely held belief that a complex blend of genetic and environmental factors is required to drive disease. In terms of clinically relevant environmental factors, the culprits that are most often mentioned and have the strongest evidentiary support are coxsackieviruses (CVBs). Evidence for CVB infection has often been described in recent-onset patients, and CVBs have a clear propensity for infecting …

miR, miR in the Cell, Does the Virus Control Them All?