Murine norovirus (MNV) was used as a surrogate to study resistance of human norovirus to disinfectants used in hospitals. MNV was sensitive to alcohol, alcohol hand rubs, bleach, and povidone iodine-based disinfectant. Real-time reverse transcription-PCR results indicated that the presence of viral RNA did not correlate with the presence of infectious virus.Human noroviruses (NoVs) are causative agents of gastroenteritis in all age classes (14). Human NoV is responsible for large outbreaks in community settings like nursing homes or hospitals, in which nosocomial infections have also been reported (11,15,29). Person-to-person, food-borne, and waterborne transmissions of NoV have been documented (11). Previous studies showed that NoVs were resistant in the environment (7,20) and suggested the risk of NoV transmission via contaminated surfaces (3, 13).The study of human NoV has been hampered by the lack of a cell culture system, as reviewed previously (9). To study resistance of human NoV to environmental factors or virucidal agents, cultivatable feline calicivirus (FCV) from the genus Vesivirus has been used as a surrogate until now (27). FCV is sensitive to ethanol, 1-propanol, and isopropanol (12, 21). FCV is also inactivated in the presence of sodium hypochlorite, chlorine dioxide, iodine, or glutaraldehyde (6,8,10,28,30). Alcohol-based hand rubs induced 1 to 2 log 10 50%-tissueculture-infective-dose reductions in the FCV titer in the presence of organic soil (16).Recently the first murine NoV (MNV) was characterized (18) and adapted to cell culture on murine macrophage-related cells (31). The MNV capsid structure, genomic organization, and replication cycle are very similar to those of human NoVs (18,26). Recently Cannon et al. showed that MNV and FCV were resistant to organic solvents and their inactivation rates were similar at 63 and 72°C (2). However, MNV was more resistant than FCV to basic and acidic pHs. Long-term resistance was also higher for MNV than for FCV at room temperature, once resuspended in stool material. Additionally, MNV could be effectively inactivated by liquid-and fog-based hypochlorous acid solutions on porous and nonporous surfaces (24). In this study, we determined whether alcohols (ethanol and isopropanol), alcohol-based hand rubs (Stérillium, Aniosgel 85NPC, and Purell), and commercial disinfectants (Asphène381, bleach, and Betadine), which are commonly used in French hospitals, could reduce the viral titer of MNV by 4 log 10 as required by European standards for virucidal efficacy, as reviewed previously (27). Plaque assay and realtime reverse transcription (RT)-PCR procedures were evaluated for the detection and the quantification of MNV.The RAW cells were maintained as described previously (31). MNV was propagated RAW cells in fetal bovine serum (FBS)-free Dulbecco's modified Eagle medium (DMEM) and harvested at 2 days postinfection. High-titer MNV stocks were prepared by ultracentrifugation of precleared MNV-infected cell lysate. For MNV titration, the cells were inoculated w...

According to the current paradigm, lymphocyte homing to the small intestine requires the expression of two tissue-specific homing receptors, the integrin α4β7 and the CCL25 receptor CCR9. In this study, we investigated the organ distribution and the homing molecule expression of IgA Ab-secreting cells (ASCs) induced by intrarectal immunization with a particulate Ag, in comparison with other mucosal immunization routes. Intrarectal immunization induces gut-homing IgA ASCs that localize not only in the colon but also in the small intestine, although they are not responsive to CCL25, unlike IgA ASCs induced by oral immunization. The mucosal epithelial chemokine CCL28, known to attract all IgA ASCs, does not compensate for the lack of CCL25 responsiveness, because the number of Ag-specific cells is not decreased in the gut of CCR10-deficient mice immunized by the intrarectal route. However, Ag-specific IgA ASCs induced by intrarectal immunization express the integrin α4β7, and their number is considerably decreased in the gut of β7-deficient mice immunized by the intrarectal route, indicating that α4β7 enables these cells to migrate into the small intestine, even without CCL25 responsiveness. In contrast, IgA ASCs induced by intranasal immunization express low α4β7 levels and are usually excluded from the gut. Paradoxically, after intranasal immunization, Ag-specific IgA ASCs are significantly increased in the small intestine of β7-deficient mice, demonstrating that lymphocyte homing is a competitive process and that integrin α4β7 determines not only the intestinal tropism of IgA ASCs elicited in GALTs but also the intestinal exclusion of lymphocytes primed in other inductive sites.

Rotavirus (RV) is the main etiological agent of severe gastroenteritis in infants, and vaccination seems the most effective way to control the disease. Recombinant rotavirus-like particles composed of the viral protein 6 (VP6) and VP2 (2/6-VLPs) have been reported to induce protective immunity in mice when administered by the intranasal (i.n.) route. In this study, we show that administration of 2/6-VLPs by the intrarectal (i.r.) route together with either cholera toxin (CT) or a CpG-containing oligodeoxynucleotide as the adjuvant protects adult mice against RV infection. Moreover, when CT is used, RV shedding in animals immunized by the i.r. route is even reduced in comparison with that in animals immunized by the i.n. route. Humoral and cellular immune responses induced by these immunization protocols were analyzed. We found that although i.r. immunization with 2/6-VLPs induces lower RV-specific immunoglobulin G (IgG) and IgA levels in serum, intestinal anti-RV IgA production is higher in mice immunized by the i.r. route. Cellular immune response has been evaluated by measuring cytokine production by spleen and Peyer's patch cells (PPs) after ex vivo restimulation with RV. Mice immunized by the i.n. and i.r. routes display higher gamma interferon production in spleen and PPs, respectively. In conclusion, we demonstrate that i.r. immunization with 2/6-VLPs protects against RV infection in mice and is more efficient than i.n. immunization in inducing an anti-RV immune response in intestinal mucosa.

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