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Journal of Virology, December 2006, p. 12377-12386, Vol. 80, No. 24
0022-538X/06/$08.00+0     doi:10.1128/JVI.01185-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Rotavirus Infection Enhances Lipopolysaccharide-Induced Intussusception in a Mouse Model

Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas 77030,¹ United States Army Medical Research Insititute of Infectious Diseases, 1425 Porter Street, Fort Detrick, Maryland 21702,² Department of Gastrointestinal Sciences, Christian Medical College and Hospital, Vellore 632 004, India,³ Veterans Affairs Medical Center, 2002 Holcombe Boulevard, Houston, Texas 77030⁴

Received 7 June 2006/ Accepted 15 September 2006

Unexpected reports of intussusception after vaccination with the live tetravalent rotavirus vaccine RotaShield resulted in voluntary withdrawal of the vaccine. Intussusception, a condition in which the intestine acutely invaginates upon itself, is the most common cause of intestinal obstruction in children. We report here the development of a mouse model to study rotavirus-induced intussusception. In this model, both homologous murine and heterologous simian rotavirus strains significantly enhanced the rate of lipopolysaccharide (LPS)-induced intussusception, and this enhancement was replication dependent, requiring rotavirus doses of greater than one 50% infectious dose. Rotavirus-induced intussusceptions did not have observable lymphoid lead points, despite the induction of intestinal lymphoid hyperplasia after rotavirus infection. Intussusceptions are also postulated to result from altered intestinal motility, but rotavirus infection had no effect on gastrointestinal transit. LPS-induced intussusception is associated with the induction of inflammatory mediators, and intussusception rates can be modified by inflammatory antagonists. We show that rotavirus infection significantly enhanced serum tumor necrosis factor alpha and gamma interferon cytokine levels after LPS treatment compared to uninfected mice. Together, these data suggest that rotavirus infection sensitized mice to the inflammatory effects of subsequent LPS treatment to enhance intussusception rates.

Published ahead of print on 27 September 2006.

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