title: Enteroviruses as causative agents in type 1 diabetes: loose ends or lost cause?
abstract: 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 β 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 β cell response to the establishment of a persistent enteroviral infection determines the final disease outcome.
authors.affiliation: Institute of Biomedical and Clinical Science, University of Exeter Medical School, RILD Building, Barrack Road, Exeter EX2 5DW, UK. Electronic address: n.g.morgan@exeter.ac.uk.
authors.forename: Noel G
authors.initials: NG
authors.lastname: Morgan
authors.affiliation: Institute of Biomedical and Clinical Science, University of Exeter Medical School, RILD Building, Barrack Road, Exeter EX2 5DW, UK. Electronic address: s.richardson@exeter.ac.uk.
authors.forename: Sarah J
authors.initials: SJ
authors.lastname: Richardson
mesh_terms: D000818:Animals; D003922:Diabetes Mellitus, Type 1 / Q000473:pathology* / Q000821:virology*; D004770:Enterovirus / Q000472:pathogenicity*; D006801:Humans; D050417:Insulin-Secreting Cells / Q000473:pathology / Q000821:virology; D007515:Islets of Langerhans / Q000166:cytology
keywords: Coxsackievirus; islets of Langerhans; pathogen recognition receptors; persistent infection; type 1 diabetes