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*
Department of Medicine, Northport Veterans Affairs Medical Center, Northport, NY 11768;
Department of Pathology, State University of New York, Stony Brook, NY 11794;
Laboratoire de Virologie et d’Immunologie Moleculaire, Institut National de la Recherche Agronomique, C. R. J. Domaine de Vilvert, Jouy-en-Josas, France; and
§
Departments of Medicine and Microbiology, Palo Alto Veterans Affairs Medical Center and Stanford University, Stanford, CA 94305
Rotavirus is the most important worldwide cause of severe
gastroenteritis in infants and young children. Intestinal epithelial
cells are the principal targets of rotavirus infection, but the
response of enterocytes to rotavirus infection is largely unknown. We
determined that rotavirus infection of HT-29 intestinal epithelial
cells results in prompt activation of NF-
B (<2 h), STAT1, and ISG
F3 (3 h). Genetically inactivated rotavirus and virus-like particles
assembled from baculovirus-expressed viral proteins also activated
NF-B. Rotavirus infection of HT-29 cells induced mRNA for several
C-C and C-X-C chemokines as well as IFNs and GM-CSF. Mice infected with
simian rotavirus or murine rotavirus responded similarly with the
enhanced expression of a profile of C-C and C-X-C chemokines. The
rotavirus-stimulated increase in chemokine mRNA was undiminished in
mice lacking mast cells or lymphocytes. Rotavirus induced chemokines
only in mice <15 days of age despite documented infection in older
mice. Macrophage inflammatory protein-1ß and IFN-stimulated protein
10 mRNA responses occurred, but were reduced in p50-/-
mice. Macrophage inflammatory protein-1ß expression during rotavirus
infection localized to the intestinal epithelial cell in murine
intestine. These results show that the intestinal epithelial cell is an
active component of the host response to rotavirus
infection.
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