Type 1 (insulin-dependent) diabetes is a typical organ-specific autoimmune disease where insulin-producing beta cells are destroyed by immune mediated mechanisms. The risk of the disease is modulated by genetic factors, mainly genes coding for human leukocyte antigens (HLA), but environmental factors are needed to trigger the process in genetically susceptible individuals. Possible viral triggers of the disease have been sought for years but their identification has been very difficult. Recently, considerable progress has been made by employing new research methods which have supported the idea that the group of enteroviruses may be particularly important in the pathogenesis. An association between enterovirus infections and type 1 diabetes was first reported 30 years ago and since then evaluated in several studies. Recent molecular studies have considerably strengthened this hypothesis by showing that enterovirus genome is present in the blood of diabetic patients. In addition, the first prospective studies have suggested that enterovirus infections may initiate the beta-cell damaging process several years before clinical diabetes is diagnosed. Ecological studies have also indicated similarities in the epidemiology of type 1 diabetes and poliomyelitis - a well-known enterovirus disease. Experimental models, like enterovirus-infected mice or in vitro-cultured beta cells, have provided important information about possible mechanisms, but still it is not known how beta cells are destroyed in human beings. The ongoing prospective studies will answer many open questions, and should the association still hold true, intervention trials will be needed to confirm causality. Even if enterovirus infections were not associated with all diabetes cases but rather with a subgroup of them, this would offer attractive possibilities to prevent the disease or part of it, for example, by an enterovirus vaccine.