Purpose of review: It is the current opinion that pathogens, such as viruses, are contributing to the development of type 1 diabetes (T1D) in susceptible individuals. This opinion is based on epidemiological associations, direct isolation of pathogens from the islets of Langerhans, as well as a large amount of data from various experimental animal models. Human enteroviruses have dominated the literature associated with the etiology of T1D. However, virus infections have also been reported to protect from autoimmune disorders.
Recent findings: Here we review the evidence for virus infections to be involved in the pathogenesis of T1D and discuss potential mechanisms of how such infections could accelerate the destruction of insulin-producing β-cells. In addition, we will review evidence from epidemiologic and experimental animal studies showing that virus infections could also have protective properties.
Summary: Virus infections play an important role in the pathogenesis of T1D by inducing or accelerating the autodestructive process, but also by protecting from autoimmunity. Thus, multiple sequential infections might shape the autoreactive immune repertoire and the pathogenesis of T1D in a complex fashion.