The activation and maintenance of pulmonary viral disease is regulated at multiple levels and determined by the early innate response to the pathogenic stimuli. Subsequent activation events that rely directly and indirectly on the virus itself can alter the development and severity of the ensuing immunopathologic responses. In the present review we outline several interconnected mechanisms that rely on the early recognition of viral nucleic acid for the most appropriate anti-viral immune responses, including TLRs and Notch activation in DCs and T cells. Deviation or persistence of the immune response to respiratory viruses may impact significantly on the severity of the responses. While these mechanisms are likely similar in most respiratory viral infections, this review will focus on findings with respiratory syncytial virus (RSV) infections.