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Trends Endocrinol Metab. 2014 Dec;25(12):611-9. doi: 10.1016/j.tem.2014.08.002. Epub 2014 Aug 28.

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

Author information

1
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.
2
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.

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.

KEYWORDS:

Coxsackievirus; islets of Langerhans; pathogen recognition receptors; persistent infection; type 1 diabetes

PMID:
25175301
DOI:
10.1016/j.tem.2014.08.002
[Indexed for MEDLINE]

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