Possible reasons for the discrepancies between these studies are infection with different virus doses and strains, including those with unusual tissue tropism such as WSN, and usage of either IFNαβR−/− or signal transducer and activator of transcription1−/− (STAT1−/−) mice as models of IFN signalling deficiency on C57BL/6, 129Sv/Ev, CD1 or mixed mouse backgrounds, making comparisons within and between studies difficult. Here, IFNAR2 is linked to infection.