Figure 1.

Putative mechanisms for initiation of islet autoimmunity (IA) and acceleration to type 1 diabetes (T1D) by viruses: (1) Direct infection and β-cell cytolysis; (2) Bystander activation; (3) Dysregulation of host miRNAs; (4) Molecular mimicry; and (5) Persistent infection. These mechanisms are not mutually exclusive and likely act in interacting pathways to trigger IA and/or facilitate progression of T1D pathogenesis [107,137]. However, there is little direct mechanistic evidence from humans, with poor understanding of how virus-induced insulitis may involve into a targeted autoimmune attack [102]. Abbreviations: MHC, major histocompatibility complex.