Human Noroviruses (HuNoVs) are single stranded RNA (ssRNA) viruses belonging to Caliciviridae family which are the major cause of non-bacterial gastroenteritis globally. In 2003, the first mouse norovirus (MNV) was discovered, which displays a tropism for macrophage-like cells in vivo and replicates in macrophages and dendritic cells cultured in vitro. Studies of MNV have revealed that all three interferon (IFN) signaling pathways (Type I, II and III) are involved in host recognition and antiviral signaling against norovirus infection through JAK-STAT signaling pathway. However only cytoplasmic Melanoma Differentiation-Associated protein 5 (MDA5) and to a lesser extent endosomal Toll-like receptor 3 (TLR3) has been shown to play a role in the induction of cytokines in response to MNV infection in mice. We hypothesised that Tlr7, another endosomal receptor involved in detection of ssRNA viruses including influenza A, is involved in Norovirus RNA sensing. Our preliminary data suggested an increase in the induction of proinflammatory cytokines in response to MNV infection, in Tlr7-deficient bone marrow-derived macrophages (BMMs) compared to WT BMMs. Quantification of viral titers and MNV RNA levels also showed a statistically significant reduction in viral replication in Tlr7-deficient BMMs. Collectively our results suggest a novel beneficial role of Tlr7 for MNV replication and contrary to its classical function, Tlr7 can be utilized by MNV to avoid swift innate immune degradation.