. RSV F protein causes TLR4-mediated NF-κB activation during the early infection stages of infection that is dependent upon virus replication. IL-1β, IL-6, and IL-8 are induced via NF-κB activated by the stimulation of TLR4. During the late stages, the viral G protein is produced, and secreted, which then suppresses TLR4-mediated signal transduction [46] . The cysteine-rich (GCRR) region of the G protein is also important for NF-κB suppression. Following the interaction of virus proteins with host cell surface proteins, the viral M2-1 protein inhibits the translocation of RelA, a component of NF-κB, to the cell nucleus [47] . Expression of the viral nonstructural proteins, NS1 and NS2 inhibit activation of IRF3 induced by TLR3, TLR4, and RIG-I signaling, and also suppress IFN production [48] . However, NS1 and NS2 proteins have little effect on NF-κB or AP-1 activation, so the production of proinflammatory cytokines may be effectively induced in the RSV-infected cells.