Furthermore, as reported previously for wild-type mice (Barton et al., 2007), MHV68 latency enhanced the ability of peritoneal macrophages from control and HOIL-1 KO mice to kill Listeria. Together, these data suggest that the constant presence of low levels of IFNγ driven by latent virus infection results in an increase in the basal expression levels of downstream effector molecules and the priming of cells for the enhanced immediate killing of Listeria upon infection, as well as for a more rapid further induction of IFNγ and its effector molecules in response to the bacterial challenge. This evidence concerns the gene IFNG and infection.