Peripheral pDCs likely represent a significant source of the systemic IFNα observed following in vivo rotavirus infection [43], [72], [73], [74]; the dispensability of proteolytic activation of VP4 for pDC infection and IFNα stimulation by rotavirus provides a mechanism for the establishment of the antiviral state extraintestinally by a small amount of virus. The gene discussed is IFNA1; the disease is Rotavirus infection.