In the mouse infection model, the RSV F protein was reported to be an effector to trigger the production of IFN-β via interaction with TLR4 (Kurt-Jones et al., 2000; Haynes et al., 2001); while in monocyte-derived dendritic cells (mDCs), the soluble G protein was demonstrated to inhibit TLR3/4-mediated IFN-β production (Shingai et al., 2008). The gene discussed is TLR3; the disease is infection.