[Coxsackievirus B infection and pathogenesis of type 1 diabetes].

Epidemiological and experimental studies suggest that enteroviruses (EV) and particularly coxsackieviruses B (CVB) 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 CVB in the pathogenesis of T1D. CVB can infect and persist in the intestine, thymic cells, monocytes/macrophages, ductal cells and pancreatic β-cells, which leads to structural or functional alterations of these cells. A chronic inflammatory response and disruption of tolerance towards β-cells due to CVB infections are able to promote the recruitment and activation of pre-existing autoreactive T-cells and the destruction of β-cells. Vaccine or therapeutic strategies to control EV infections have been developed and open perspectives for the prevention or treatment of T1D.