Abstract
Organ-specific autoimmunity frequently affects the endocrine system, including pancreatic islets. Type 1 diabetes mellitus (T1D) derives from the autoimmune destruction of insulin-secreting β-cells that is triggered by environmental factors (1, 2). Genetic predisposition accounts for 36–50% of disease susceptibility as demonstrated in monozygotic twin studies (3–5). Approximately 90% of new cases lack a family history of T1D indicating a large contribution of exogenous factors to pathogenesis. A variety of associations with viral infections have been reported for human diabetes including rubella, mumps, and cytomegalovirus. However, among investigated agents, human enteroviruses (HEVs) appear to play a prominent role (1). HEVs are extremely common RNA viruses that spread mainly through the fecal-oral route. Overall, these agents cause millions of new infections per year worldwide (6). The enterovirus genus comprises over 100 antigenically different virus types (7). The single-stranded 7.5 kb RNA enteroviral genome encodes for capsid proteins and other proteins involved in viral infectivity and replication. Capsid proteins are highly variable among HEV species and types. Neutralizing antibodies raised against capsid proteins are highly type specific but may also cross-react with related types (8). So far, there are no means for preventing T1D. Sets of well-defined autoantibodies have a strong predictive value (9, 10), but the costbenefit ratio of periodical determinations appears not to justify screening programs at the population level. At the diagnosis of T1D, a small fraction Oscar Diaz-Hortaa,c, Andreina Baja, Giuseppe Maccaria, Alessandro Salvatonib and Antonio Tonioloa aDepartment of Experimental Medicine, Laboratory of Medical Microbiology, University of Insubria, Varese, Italy; bDepartment of Experimental Medicine, Pediatric Endocrinology Unit, University of Insubria, Varese, Italy; and cDepartment of Immunology and Genetics, National Institute of Endocrinology, Havana, Cuba
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