The outcome of a viral infection is determined by the balance between host antiviral defenses and viral evasion strategies. To achieve the best possible outcome during infection the host utilizes pattern recognition receptors (PRRs) to rapidly and specifically detect the presence of an invading virus. One class of PRRs, the RLRs, integrate two distinct signals; cytoplasmic RNA and virus-induced cytoskeletal changes to reliably and quickly promote an antiviral response mediated by interferons (IFNs), which induce the expression of interferon stimulated genes (ISGs). On the other hand, viruses such as murine norovirus (MNV) have evolved to combat the host immune response by encoding multifunction proteins, such as NS5, which can inhibit the host's IFN response by preventing the activation of the critical signal transducer STAT1. An understanding of the interplay between the host immune response and the corresponding mechanisms of viral subversion can help us tip the balance in favor of host survival by developing therapeutics that bolster the immune response or inhibit viral immune antagonists.