Viruses and Type 1 Diabetes: Focus on the Enteroviruses

Type 1 diabetes (T1D) is one of the most common chronic diseases in developed countries and represents about 10% of all cases of diabetes. It is caused by a selective destruction of insulin-producing β cells in the pancreas. The disease has two subtypes: 1A, which includes the common, immune-mediated forms of the disease; and 1B, which includes nonimmune forms. In this review, we focus on subtype 1A, which for simplicity will be referred to as type 1 diabetes. [81, 34]. An increasing incidence rate of T1D has been observed for the last few decades especially in young individuals (less than five years old) [163]. The cause of T1D is still unknown. Several factors interact and lead to the development of the disease. An inflammatory islet infiltrate (insulitis) can be observed at the symptomatic onset of T1D, and reflects the immune response to β-cells [45]. T1D is an autoimmune disease, which implies a role of immune response effectors in the pathogenic processes and a failure of tolerance to‐ wards β-cell antigens.The susceptibility to T1D is influenced by genetic factors. More than 20 loci in addition to those located in the human leukocyte antigen (HLA) class II locus (es‐ pecially DQ and DR) on chromosome 6 are involved. Another contribution to the pathogen‐ esis of the disease could rely on epigenetic modifications (such as DNA methylation) and parent-of-origin effects [11]. Genetic modifications in the population cannot explain the rap‐ idly increased incidence of T1D in most populations. Altogether, the incidence variation from one season to another, the relationship between immigration and disease develop‐ ment, and the differences in incidence in different parts of the world in neighboring popula‐ tions with similar genetic profiles, suggest that the disease is a result of interaction of genetic and environmental factors [94].