The finding that IFN-I responses within the OB are not significantly affected by MAVS deletion in long-lived CX3CR1+ cells together with the observation that CX3CR1-CreER± MAVSfl/fl mice succumb to the infection at the time point when T-cell responses are needed to restrict virus propagation imply that cell–cell communication between microglia and infiltrating T cells is critically relevant. Here, MAVS is linked to infection.