Cytomegalovirus (CMV) is highly prevalent amongst the human population. Although it is largely asymptomatic, immunocompromised individuals can experience adverse disease symptoms. In pregnancy, it can be transmitted to the fetus and remains the most common cause of congenital infection. Murine cytomegalovirus (MCMV) provides a well-established model of human cytomegalovirus (HCMV) and is recognised at an innate level by toll-like receptors (TLRs) 7 and 9 in the mouse. We also propose that the ASC-containing inflammasome could prove important in the production of pro-inflammatory cytokines during MCMV recognition. In order to investigate these innate immune sensing pathways and the process by which MCMV infection is controlled, we have generated a mouse which is deficient for the innate TLRs 7 and 9 and the inflammasome adaptor molecule ASC (TLR7/9/ASC KO). These mice display an abrogated pro-inflammatory cytokine response to viral challenge in vitro, and display greater viral load in vivo in comparison to their wildtype counterparts suggesting this innate signalling is important in the control of viral infection. However, cytotoxic T cell and antibody responses to MCMV are comparable in both mice, suggesting the adaptive arm is not interrupted by a lack of innate signalling. Additionally, NK cell mediated cytotoxicity will be assessed to determine whether the absence of innate cytokines directly influences killing of MCMV infected cells. This data will for the first time display the synergism of TLR signalling and inflammasome activation in the host response to MCMV challenge and thus provide information as to the responses which may be effected in models of MCMV infection.