However, our data suggest that IFN-I signaling did not mediate the increased viral control in Mtb-infected lungs, as we showed that Ifnar1-/- mice had a similarly reduced SCV2 burden as WT mice when previously infected with Mtb. Nevertheless, we also showed that IFNAR1-deficient mice had a higher viral load at 3 days post-infection independently of Mtb infection status, in line with previously published in vivo data that support IFN-I-dependent control of SCV2 replication in mice (53–57) and hamsters (58, 59). Here, IFNAR1 is linked to infection.