To exclude the possible role of TRIM29-regulated type I IFN in the antiviral phenotype during intestinal infection of enteric viruses, we used Ifnar1 (type I IFN receptor) knockout (Ifnar1−/−) mice and crossed them with Trim29fl/fl and Trim29IEC-KO mice to generate Ifnar1−/−Trim29fl/fl and Ifnar1−/−Trim29IEC-KO mice. The gene discussed is TRIM29; the disease is digestive system infectious disorder.