Ly49H triggering by m157 is required for the proliferation and accumulation of NK cells between days 3 and 7 after MCMV infection [28] . Therefore, we first used NK cell expansion as an indicator to show that Klra8 and BALB/c mice generate an NK cell response of different quality to MCMV infection ( Figure S1A ). We next compared the ability of Klra8 and BALB/c mice to control early viral load. Consistent with reported differences in viral load seen between mice lacking or possessing the Ly49H gene [26, 29, 30] , there was a substantially higher viral burden within the spleens of BALB/c mice when compared to those of congenic Klra8 animals ( Figure S1B ). In addition, NK cell depletion in Klra8 mice increased viral replication to levels similar to those observed in BALB/c animals ( Figure S1C ). Thus, these data confirm previous reports demonstrating that Klra8 mice mount a strong NK cell response that is able to efficiently control MCMV replication, in contrast to BALB/c animals.