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J. Virol. doi:10.1128/JVI.00942-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Astrovirus Increases Epithelial Barrier Permeability Independently of Viral Replication

Department of Medical Microbiology and Immunology, University of Wisconsin-Madison, Madison, WI 53706; School of Biomedical and Molecular Sciences, University of Surrey, Guildford, Surrey, GU2 7XH

^* To whom correspondence should be addressed. Email: slschul2{at}wisc.edu.

	Abstract

Astrovirus infection in a variety of species results in an age-dependent diarrhea; however, the means by which astroviruses cause diarrhea remain unknown. Studies in astrovirus infected humans and turkeys have demonstrated few histological changes and little inflammation during infection, suggesting that intestinal damage or an over-zealous immune response are not the primary mediators of astrovirus diarrhea. An alternative contributor to diarrhea is increased intestinal barrier permeability. Here, we demonstrate that astrovirus increases barrier permeability in a Caco-2 cell culture model system following apical infection. Increased permeability correlated with disruption of the tight junction protein occludin and decreased actin stress fibers in the absence of cell death. Additionally, permeability was increased when monolayers were treated with UV-inactivated virus or purified recombinant HAstV-1 capsid in the form of viral-like particles. Together, these results demonstrate that astrovirus induced permeability occurs independently of viral replication and is modulated by the capsid protein, a property apparently unique to astroviruses. Based on these data, we propose that the capsid may contribute to diarrhea in vivo.

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