Rotavirus infection is the most common cause of severe infantile
gastroenteritis worldwide. These viruses infect mature enterocytes of the small intestine and cause structural and functional damage, including a reduction in
disaccharidase activity. It was previously hypothesized that reduced
disaccharidase activity resulted from the destruction of rotavirus-infected enterocytes at the villus
tips. However, this pathophysiological model cannot explain situations in which low
disaccharidase activity is observed when rotavirus-infected intestine exhibits few, if any, histopathologic changes. In a previous study, we demonstrated that the simian rotavirus strain RRV replicated in and was released from human enterocyte-like Caco-2 cells without cell destruction (N. Jourdan, M. Maurice, D. Delautier, A. M. Quero, A. L. Servin, and G. Trugnan, J. Virol. 71:8268-8278, 1997). In the present study, to reinvestigate
disaccharidase expression during
rotavirus infection, we studied
sucrase-
isomaltase (SI) in RRV-infected Caco-2 cells. We showed that SI activity and apical expression were specifically and selectively decreased by RRV
infection without apparent cell destruction. Using pulse-chase experiments and cell surface biotinylation, we demonstrated that RRV
infection did not affect SI biosynthesis, maturation, or stability but induced the blockade of SI transport to the brush border. Using confocal
laser scanning microscopy, we showed that RRV
infection induces important alterations of the cytoskeleton that correlate with decreased SI apical surface expression. These results lead us to propose an alternate model to explain the pathophysiology associated with
rotavirus infection.