Abstract

Type 1 diabetes (T1D) is a multifactorial autoimmune disease for which viral infections have potential pathogenic mechanisms. Recent studies have given more attention to enteroviruses (EV ) whose infections during childhood can cause formation of islet autoantibodies. Thus, coxsackie viruses, which belong to genus EV, can induce autoimmunity through molecular mimicry or
through changing Th1 immune response. This mechanism is further amplified by the interferon pathway that is activated during viral infections. In addition to EV, other viruses have been studied as well. The role of cytomegalovirus in progression of T1D is still not fully understood and studies have led to contradictory results. Parechovirus A is thought to have a protective effect in T1D
progression and parechovirus B is thought to be associated with formation of autoantibodies. Still, the results of existing studies are contradictory and do not allow to make definite conclusions. Rotavirus infections before the age of 6 months can increase the likelihood of autoantibody formation. Rubella infection during pregnancy can cause congenital rubella syndrome, which increases the risk of the child acquiring T1D.