Recently, it was reported that rotavirus infection in infant mice induced apoptosis in vivo [7] . Although DNA analysis showed that the majority of cells present in infected mucosal scrapings were not apoptotic, we observed upregulation of the apoptosis effector protein CASP3. This suggests that programmed cell death in the epithelial layer was stimulated by rotavirus infection. NB analysis detected a considerable level of CASP3 mRNA expression in uninfected mucosal scrapings. This constitutive expression of CASP3 is, most likely, related to the process of maintenance of the absorptive status of the intestinal epithelial layer. A process in which mature enterocytes continually die due to apoptosis and are replaced by differentiating cells migrating from surrounding crypts to the tip of the villi [20] . In contrast to mature enterocytes, an in vivo study in mice showed that goblet cells are largely spared from apoptosis in rotavirus-infected mice [8] . Moreover, migration of goblet cells from the crypt to the tips of the villi was stimulated in these mice. We found up-regulation of the goblet cell marker gene KRT20 [51] and the lower and mid-villus immature enterocyte marker gene MGAM [42] . This could indicate that transcriptional activity in both of these cell types was promoted. Stimulation of apoptosis in rotavirus-infected enterocytes and higher proliferation/differentiating activity in goblet cells and immature enterocytes could be a coordinated response of the jejunum to remove infected enterocytes and overlay villus tips with fresh enterocytes, goblet cells, and mucus layer. We did not detect genes on our array that were directly associated with cell-cycle progression/arrest. However, down-regulation of the nuclear kinase FRK (an antagonist of cell proliferation) and TMS4F20 may be associated indirectly with this process. In humans, TMS4F20 is strongly homologous to TM4SF4, a protein that reduced the ability of the crypt cell line HT29 to proliferate [48] .