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Defining the role of viruses in the aetiopathogenesis of human type 1 diabetes has been an elusive goal for more than 40 years, although indirect evidence is mounting that viruses have an important modulatory role in the development of the disease through their interaction with the innate immune system. In this issue of Diabetologia, Willcox et al. provide histopathological evidence that the islets of Langerhans in seven young patients with recent-onset disease expressed the enteroviral protein VP1 and report that this marker is preferentially present in islets that show signs of enhanced replicative activity. They suggest that insulitis may be the common factor linking beta cell replication and VP1 positivity, with persistent virus infection leading to chemokine secretion, infiltration of immune cells (insulitis) and pro-inflammatory cytokine-induced beta cell replication.

Insulitis in the human endocrine pancreas: Does a viral infection lead to inflammation and beta cell replication?