November 29, 2013

The gastrointestinal frontier: IgA and viruses



Front. Immunol., 28 November 2013 | doi: 10.3389/fimmu.2013.00402


  • Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX, USA
Viral gastroenteritis is one of the leading causes of diseases that kill ~2.2 million people worldwide each year. IgA is one of the major immune effector products present in the gastrointestinal tract yet its importance in protection against gastrointestinal viral infections has been difficult to prove. In part this has been due to a lack of small and large animal models in which pathogenesis of and immunity to gastrointestinal viral infections is similar to that in humans. Much of what we have learned about the role of IgA in the intestinal immune response has been obtained from experimental animal models of rotavirus infection. Rotavirus-specific intestinal IgA appears to be one of the principle effectors of long term protection against rotavirus infection. Thus, there has been a focus on understanding the immunological pathways through which this virus-specific IgA is induced during infection. In addition, the experimental animal models of rotavirus infection provide excellent systems in which new areas of research on viral-specific intestinal IgA including the long term maintenance of viral-specific IgA.











Keywords: IgA, rotavirus, calicivirus, norovirus, adenovirus, astrovirus, small intestine, gastrointestinal virus
Citation: Blutt SE and Conner ME (2013) The gastrointestinal frontier: IgA and viruses.Front. Immunol. 4:402. doi: 10.3389/fimmu.2013.00402
Received: 21 May 2013; Paper pending published: 07 June 2013;
Accepted: 08 November 2013; Published online: 28 November 2013.
Edited by:
Nils Yngve Lycke, University of Gothenburg, Sweden
Reviewed by:
Artur Summerfield, Institute of Virology and Immunoprophylaxis, Switzerland
Nicolaas Adrianus Bos, University Medical Center Groningen, Netherlands
Copyright: © 2013 Blutt and Conner. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Margaret E. Conner, Department of Molecular Virology and Microbiology, Baylor College of Medicine, Room 936E, One Baylor Plaza, MSC BCM 385, Houston, TX 77030, USA e-mail: mconner@bcm.edu

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