Format

Send to

Choose Destination
See comment in PubMed Commons below
Nat Rev Endocrinol. 2010 May;6(5):279-89. doi: 10.1038/nrendo.2010.27. Epub 2010 Mar 30.

Pathogenesis of type 1 diabetes mellitus: interplay between enterovirus and host.

Author information

  • 1Laboratoire de Virologie/EA3610 "Pathogenèse Virale du Diabète de Type 1", Faculté de Médecine, Université Lille 2, CHRU Lille, Centre de Biologie et Pathologie et Institut Hippocrate Parc Eurasanté, Boulevard du Prof J Leclercq, 59037 Lille Cedex, France.

Abstract

Enteroviruses are believed to contribute to the pathogenesis of type 1 diabetes mellitus (T1DM). In this Review, the interplay between infection with enteroviruses, the immune system and host genes is discussed. Data from retrospective and prospective epidemiological studies strongly suggest the involvement of enteroviruses, such as coxsackievirus B, in the development of T1DM. Enteroviral RNA and/or proteins can be detected in tissues of patients with T1DM. Isolation of coxsackievirus B4 from the pancreas of patients with T1DM or the presence of enteroviral components in their islets strengthens the hypothesis of a relationship between the virus and the disease. Enteroviruses can play a part in the early phase of T1DM through the infection of beta cells and the activation of innate immunity and inflammation. In contrast with its antiviral role, virus-induced interferon alpha can be deleterious, acting as an initiator of the autoimmunity directed against beta cells. Enteroviruses, through persistent and/or successive infections, can interact with the adaptive immune system. Host genes, such as IFIH1, that influence susceptibility to T1DM are associated with antiviral activities. An increased activity of the IFIH1 protein may promote the development of T1DM. An improved knowledge of the pathogenic mechanisms of enterovirus infections should help to uncover preventive strategies for T1DM.

[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Nature Publishing Group
    Loading ...
    Write to the Help Desk