The urgent need to prevent type 1 autoimmune childhood diabetes.

Clinical onset of autoimmune Type 1 diabetes mellitus (T1DM) develops after an asymptomatic, complex interaction between host genetic and environmental factors lasting several years. The world-wide increase in T1DM incidence with no cure in sight necessitates the identification of the causative environmental factors in order to develop methods for preventing them from participating in the autoimmune process leading to T1DM. Human trials to prevent insulitis or development of T1DM (secondary prevention trials) have not as yet produced satisfactory outcomes despite promising results from T1DM animal models, possibly because the autoimmune response had already progressed too far and could not be stopped or reversed. Primary prevention trials conducted with individuals with increased genetic risk, but without signs of autoimmune response or metabolic abnormalities have also not yet produced any clear benefit. A correlation between month of birth and T1DM implicated seasonal infectious pathogens in the etiology of T1DM. This has prompted a search for those seasonal pathogens including viruses that might lead to onset of T1DM. Many studies investigated immediate viral triggers, e.g., viral infections at the time of clinical onset of T1DM. Fewer studies have investigated virus infections as the initial or early trigger in a cascade of events leading to development of TIDM. Seasonal virus infections of pregnant women may be transmitted in utero and induce the first damage to the developing fetus's beta-cells. The identification of specific pathogenic viruses may enable development for pregestational vaccines to diminish the incidence of childhood T1DM.