These TLR-independent but MyD88-dependent antiviral responses suggested possible redundancies among TLR signals in the liver compartment in response to MCMV infection [20, 32] . To investigate this possibility, we utilized mice containing an H412R missense mutation in the endoplasmic reticulum protein UNC93B1 to address the combined function of nucleic acidsensing TLRs in the liver during acute MCMV infection. The UNC93B1 mutation (known as 'triple d' or '3d') impairs signaling through TLR3, TLR7 and TLR9 due to improper trafficking of these receptors to the endosomal compartment, and has been shown to affect exogenous antigen presentation [34, 35] . Our studies show that proinflammatory cytokine production after early infection with MCMV is dependent on UNC93B1. Further, UNC93B1 deficiency exacerbates liver disease and increases viral burden, although MCMV-specific CD8+ T cell responses are not impaired. Collectively, these results suggest a level of redundancy within the liver to promote viral recognition by demonstrating that a combination of nucleic acid-sensing TLRs contributes to innate inflammatory responses during MCMV infection.