In the small intestine, mature enterocytes near the top of the villi are the primary target cells for virus replication [29] . Replication in these cells provokes numerous intraand extracellular pathological changes that inevitably lead to disruption of the absorptive and digestive functions of the small intestine, and consequently, to malabsorption and diarrhea. These changes include destruction of enterocyte brush borders, enterocyte vacuolization, loss and destruction of enterocytes, villus blunting and atrophy, thinning of the intestinal wall, and crypt hyperplasia (for comprehensive reviews, see [29, 39] ). However, the nature and severity of histopathological alterations in vivo can be quite different depending on the species and virulence of the rotavirus strain. There is no clear correlation between these alterations and manifestation of clinical symptoms. A systemic inflammatory response can be absent, and rotavirus infections can be asymptomatic [29, 39] . This suggests that the interplay between host and viral factors is important for determining the course of this disease. For Electronic supplementary material The online version of this article (doi:10.1007/s00705-008-0118-6) contains supplementary material, which is available to authorized users.