Studies in European population identified predisposing factorsas maternal age greater than 25 years, preeclampsia, diseaseneonatal respiratory and jaundice (especially associated with incompatibilityAB0). Protective factors were low birth weight and lowsize. However, the associations were weak, and most importantwhen the disease began before 10 years of age.
Since 1926 has been raised regarding enterovirus, by variationsseasonal onset of diabetes and epidemiological studiesas developed after Coxsackievirus infection epidemicB4 (CVB4) in 1971 on the Pribilof Islands (Alaska). However,no difference in the frequency of monitoring in DM1five years between infected and uninfected subjects. In studiesSubsequent isolation has demonstrated the ability of viralb infect and destroy cells in animal models and in human cellsin vitro, but in autopsy studies have not been shown in the formconsistent commitment by Coxsackie, Epstein-Barr, measles or cytomegalovirus (27.31).
However, functional studies have foundincreased T cell responses to protein in children CVB4DM1 after onset of the disease, including increasedIgM values, and INF to HLA molecules, as part of the responseagainst pancreatic islets. It has also been shown that infectionsenterovirus are 2 times more frequent in siblingsof patients who developed diabetes than those without diabetes, andCoxsackie antibody titers were higher inpregnant women whose children developed DM1 (27,28). It has been postulateda theory of molecular mimicry as a cause of autoimmunity,by the similarity between the protein F2C Coxsackie B4 virus and GAD (autoantigenmain DM1) and the role of apparent contributionHLA-DR3 in the susceptibility, however, the gap between the developmentof the disease and the immune activity peak limitsviral titers utility in the study of patients