Previously, we reported that mice lacking type I interferon receptor (IFNAR-/-) are susceptible to subcutaneous (s.c.)infection of wild-type YFV and display signs of viscerotropic disease similar to human YF, whereas 17D is avirulent in this model system.19 In addition, 17D-infection leads to protective immunity against wild-type YFV challenge.16 However, we and others have reported that 17D is virulent in mice lacking both type I and type II IFN receptors (IFNAGR-/-), suggesting that type II IFN is a critical attenuation factor for 17D in vivo. The gene discussed is IFNAR1; the disease is infection.