Of note, RRV replication was better controlled by type III IFNs at earliest times post infection, because increased viral transcription was detected only on 1 dpi, and was quickly suppressed by 2 dpi in Ifnar1-/- mice, whereas viral transcripts were still elevated on 2 and 3 dpi in Ifnlr1-/- mice (Fig 4D), suggesting a somewhat more prominent role of type III IFNs in controlling intestinal RV replication and this correlated with more efficient Ifnl2/3 induction by RV than those of type I IFNs (Figs 4E and 7B, and S4 Fig). Here, IFNLR1 is linked to infection.