Enteroviral Infections and Development of Type 1 Diabetes: The Brothers Karamazov Within the CVBs

  1. Guido Sebastiani
  1. Diabetes Unit, Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy; and Fondazione Umberto Di Mario ONLUS, Toscana Life Sciences, Siena, Italy
  1. Corresponding author: Francesco Dotta, francesco.dotta{at}alice.it.

Type 1 diabetes (T1D) is the result of a selective autoimmune destruction of pancreatic islet β-cells, occurring in genetically predisposed subjects, possibly triggered or accelerated by environmental agents (1). Both innate (2) and adaptive (3) immune responses are involved in islet inflammation in T1D. The role of environmental factors has become increasingly relevant, as indicated by the marked recent rise of incidence (4), impossible to explain based on genetic changes alone. One of the environmental risk factors identified by several independent studies in man and in animal models (5) is represented by enteroviral infections, which have been epidemiologically associated to T1D development (6). Enteroviruses may contribute to the pathological events leading to β-cell damage by several different mechanisms, such as virus-induced cytolysis or islet inflammation leading to subclinical β-cell destruction (7). However, it should also be taken into account that in specific settings viral infections may also protect from diabetes development (8).

In this issue, two closely related articles written by Oikarinen et al. (9) and Laitinen et al. (10) provide important information on the potential roles of enteroviruses, and more specifically of group B coxsackieviruses (CVB), in modulating susceptibility to T1D development. Neutralizing antibodies against CVBs have been measured in a longitudinal sample series from a large prospective birth cohort in Finland (9) as well as cross-sectionally in children with newly diagnosed T1D and control subjects (10) matched according to sampling time, gender, age, and country, …

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This Article

  1. doi: 10.2337/db13-1441 Diabetes vol. 63 no. 2 384-386
  1. Free via Open Access: OA