Abstract
Type 1 diabetes (T1D) is the most common chronic metabolic disorder in children. Epigenetic and environmental factors capable of altering the penetrance of major susceptibility genes or capable of increasing the penetrance of low-risk genes are currently thought to play a role in triggering autoimmunity and T1D development. This paper discusses the current knowledge of the role of viruses in T1D. Most studies that have evaluated the potential association between viral infections and T1D have indicated that it is highly likely that some of these infectious agents play a role in T1D development. However, most T1D cases are immune-mediated, and it is supposed that the initial viral infection is capable of creating, in genetically predisposed subjects, a particular condition in which chronic local inflammation occurs through the persistence of the infecting virus in pancreatic tissue and the activation of autoimmunity by means of molecular mimicry, bystander activation, or both. Theoretically, this knowledge could lead to possible prophylaxis and therapy for T1D. Further studies devoted to evaluating which infectious agents are linked to T1D and which immune mechanisms induce or protect against the disease are needed before adequate prophylactic and therapeutic measures can be developed.
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