IFNaR−/− mice also had increased intestinal permeability compared to MuAstV-infected wild-type mice, which correlated with their in vitro observations, suggesting a role for type I IFN in protecting the epithelial barrier during infection, although MuAstV-free IFNaR−/− mice would need to be generated to definitively determine the role of type I IFN signaling in intestinal permeability [62]. Here, IFNAR1 is linked to infection.