Group B coxsackieviruses and autoimmunity: focus on Type 1 diabetes

Group B coxsackieviruses (CVB) and/or their components have been found in the blood and pancreas of patients with Type 1 diabetes (T1D). CVB infections lead to the activation of the innate and adaptive immune systems, which can result in the induction or aggravation of autoimmune processes. Persistent and/or repeated infections of pancreas islet β cells with CVB and the resulting production of IFN-α and inflammatory mediators, combined with a predisposed genetic background, may induce bystander activation of autoimmune effector T cells and an autoreactive response to islet self-antigens through molecular mimicry. Moreover, the antibody-dependent enhancement of CVB infection of monocytes, as well as infection of the thymus can intervene in the pathogenesis of T1D. In contrast with the deleterious effect of CVB, it has been shown that these viruses can protect against the development of T1D under certain experimental conditions. The role of CVB in autoimmunity is complex, and therefore a better understanding of the inducer versus protective effects of these viruses in T1D will help to design new strategies to treat and prevent the disease.