Abstract
Antibodies can prevent viruses from infecting target cells, but antibodies against viruses can also enhance the infection of target cells. This phenomenon is called antibody-dependent enhancement (ADE) of infection. The mechanisms of ADE of infection and the results of this phenomenon in vivo are discussed. The ADE of CVB infection has been observed in animal models. In the human system it has been shown in vitro that CVB4, in combination with non-neutralizing antibodies, can infect human monocytes and stimulate the production of IFN-a by these cells through interactions with a specific viral receptor (CAR) and receptors for the Fc portion of IgG (FcgRII and FcgRIII). It cannot be excluded that the ADE of CVB infection in humans can increase the infection of peripheral blood mononuclear cells by these viruses, can cause viral escape from the immune response, and may contribute to the spread of CVBs in the host. Therefore, antibodies enhancing CVB infection may play a role in the pathogenesis of type 1 diabetes induced by or associated with these viruses.
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Acknowledgements
The authors thank Delphine Caloone for technical assistance and all their collaborators. The studies performed by the authors or in progress have been or are supported by EU FP6 Integrated Project EURO-THYMAIDE (Contract LSHB-CT-2003-503410), EU FP7 PEVNET Project (FP7-HEALTH-2010-single-stage No. 261441), a grant from Nord-Pas-de-Calais Région (ArCir convention 2004/018), CHRU Lille, the Ministère de l’Education Nationale de la Recherche et de la Technologie, Université de Lille 2, France, and the Comité mixte de Coopération Universitaire Franco-Tunisien (CMCU 2008 N808/G0808). Didier Hober was awarded the 2008 prize of the Fondation pour la Recherche Médicale.
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Hober, D., Sane, F., Riedweg, K., Desailloud, R., Goffard, A. (2013). Antibody-Dependent Enhancement of Coxsackievirus-B Infection: Role in the Pathogenesis of Type 1 Diabetes. In: Taylor, K., Hyöty, H., Toniolo, A., Zuckerman, A. (eds) Diabetes and Viruses. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-4051-2_30
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