Enteroviruses as causative agents in type 1 diabetes: loose ends or lost cause?

摘要

Considerable evidence implies that an enteroviral infection may accelerate or precipitate type 1 diabetes (T1D) in some individuals. However, causality is not proven. We present and critically assess evidence suggesting that islet beta cells can become infected with enterovirus, and argue that this may result in one of several consequences. Occasionally, a fully lytic infection may arise and this culminates in fulminant diabetes. Alternatively, an atypical persistent infection develops which can be either benign or promote islet autoimmunity. We propose a model in which the 'strength' of the beta cell response to the establishment of a persistent enteroviral infection determines the final disease outcome.