Enterovirus infection, β-cell apoptosis and type 1 diabetes
Sandhya Nair A B F , Ammira Akil A C G and Maria E Craig A B C D E H
+ Author Affiliations
- Author Affiliations
A Virology Research Laboratories, POWH and UNSW Research Laboratories, South Eastern Area Laboratory Services, Prince of Wales Hospital, Sydney
B School of Biotechnology and Biomolecular Science, Faculty of Science, University of New South Wales
C School of Women’s and Children’s Health, University of New South Wales
D Institute of Endocrinology and Diabetes, The Children’s Hospital at Westmead
E Discipline of Paediatrics and Child Health, University of Sydney
F Tel: +61 2 9382 9242, Email: z3267450@student.unsw.edu.au
G Tel: +61 2 9382 9096, Email: ammira.akil@sesiahs.health.nsw.gov.au
H Tel: +61 2 9845 3907, Email: m.craig@unsw.edu.au
Microbiology Australia 34(3) 153-156 https://doi.org/10.1071/MA13051
Published: 4 September 2013
Abstract
Type 1 diabetes (T1D) results from a complex interplay between genetic and environmental factors, leading to chronic immune mediated destruction of pancreatic β-cells. The inflammatory process is initiated by one or more environmental triggers, such as a viral infection, stimulating release of autoantigens, inflammatory mediators including cytokines and chemokines, and death effectors, with resultant β-cell loss. While multiple enterovirus (EV) serotypes demonstrate β-cell tropism, most studies support a role for the coxsackievirus B (CVB) group in the pathogenesis of T1D. Experimental studies using animal models, insulin-producing cell lines and human islets indicate that the major mechanism of EV-induced β-cell destruction is apoptosis.
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