Both melanoma differentiation-associated gene 5 (MDA5)-and mitochondria antiviral-signaling protein (MAVS)-mediated type I IFN signaling pathways have been implicated in the response to CVB3 infections, and mice deficient in either TIR-domain-containing adapter-inducing interferon-β (TRIF) or MAVS show an enhanced susceptibility to viral infection [11]. Here, MAVS is linked to viral infectious disease.