Conventional mouse models are not susceptible to hepatitis A virus (HAV) because murine adaptor protein MAVS is not efficiently cleaved by HAV protease precursors, so intact type I interferon (IFN) signaling blocks productive infection. However, IFN receptor knockout (KO) mice are susceptible to HAV infection and show hallmark features of the infection, having recently been identified as a potential disease model. Researchers from Genematrix Inc. aimed to determine whether nonclinical efficacy studies can be performed in small animal models.