Despite that lung virus titers and distribution and numbers of virus antigen-positive cells were not different between untreated WT and Ifnar−/− animals, significant induction of IFN-β and CCL2 that peaked at 48 h after infection in untreated WT mice were not observed, and infiltration of CCR2+ inflammatory monocyte-derived macrophages peaking at PID 3 in WT mice was drastically reduced in mice lacking type I IFN signaling. Here, CCL2 is linked to infection.