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Epidemiological and experimental studies suggest that enteroviruses (EVs), particularly coxsackieviruses B (CVBs), are likely to trigger or accelerate the onset of islet autoimmunity and the development of type 1 diabetes (T1D) in genetically susceptible individuals. Several mutually non-exclusive mechanisms have been proposed to explain the involvement of CVBs in the pathogenesis of T1D. CVBs can infect and persist in the intestine, thymic cells, monocytes/macrophages, ductal cells, and pancreatic β-cells, leading to structural or functional alterations of these cells. A chronic inflammatory response and disruption of tolerance toward β-cells due to CVB infections encourage the recruitment and activation of pre-existing autoreactive T-cells and the destruction of β-cells. Vaccines and therapeutic strategies to control EV infections have been developed and open up possibilities for the prevention or treatment of T1D.