OBJECTIVE: Respiratory syncytial virus (RSV) and rhinovirus (RV) are common viral infections that may result in post-viral airway/atopic disease. By understanding the antiviral immune response involved, and the mechanisms that translate/associate with post-viral airway disease, further research can be directed to potential treatments that affect these mechanisms. DATA SOURCES: Utilized peer-reviewed manuscripts listed in PubMed that had relevance to RSV/RV and development of atopic/airway disease in both humans and mice. STUDY SELECTIONS: Studies that explained the mechanisms behind antiviral response were selected. RESULTS: RSV infections have been associated with post-viral airway disease primarily in those without preexisting atopy; however, the mechanistic link connecting the viral infection with atopy is less clear. Mouse models (in particular those using Sendai virus, a virus related to RSV) provide a potential mechanistic pathway that may explain the linkage between RSV and post-viral airway disease. RV infection also can drive post-viral airway disease, but unlike RSV, this seems to occur only in those with preexisting atopy. Studies explore this link by demonstrating an impaired interferon response in atopic individuals, which may make them more susceptible to development of post-viral airway disease with RV infection. CONCLUSION: Both RSV and RV are associated with a risk for developing post-viral airway disease and atopy. However, the mechanisms that connect these viruses with post-viral disease appear to be disparate, suggesting that treatments to prevent post-viral airway disease may need to be specific to the viral etiology.