The IFN-c-inducible GBP-2 gene was up-regulated 18 hpi. Overexpression of GBP-1 and GBP-2 in HeLa cells and NIH 3T3 cells abrogated the cytopathogenic effect mediated by VSV and EMCV, respectively, by an unknown mechanism [3, 11] . Furthermore, it was shown that expression of murine GBP-2 in NIH 3T3 cells neutralized the cytotoxic effect of the taxane drug Paclitaxel [4] . This drug specifically stimulates polymerization of tubulins to extraordinarily stable microtubules. These stable microtubules interfere with the function of normal microtubule filaments and inevitably induce cell death [4] . The reduced expression of PRR13 we observed (discussed above) may be an indication that the formation of extraordinarily stable microtubules in intestinal epithelial cells actually takes place in response to rotavirus infection. In fact, several studies have shown that rotavirus infection induces disorganization of the cytoskeleton network and microtubule filaments in enterocytes [9, 10, 26] . Moreover, we also observed the up-regulation of the IFN-a/b-inducible gene IFI44, a cytosolic protein associated with microtubular structures, and the cytoskeleton gene ACTB. Therefore, enhanced expression of GBP-2 in specific intestinal epithelial cells could contribute to a cellular mechanism(s) that impairs and/or prevents disorganization of the microtubule filaments.