Respiratory syncytial virus (RSV) causes annual epidemics of acute respiratory disease in large part because antibody levels fall rapidly after infection. RSV is able to infect cultured dendritic cells (DCs) and persist in these cells. Given the importance of DCs in antigen presentation, RSV infection and persistence is likely to be an evolutionary adaptation that can subvert the host immune response. This study aimed to demonstrate infection and persistence of RSV in lung DCs using an in vivo model of RSV infection. Mice were infected with a modified strain of RSV which expresses a red fluorescent protein (RSV-RFP) when replicating. Clinical symptoms of infection were monitored using weight change and inflammatory cell counts from bronchoalveolar lavage, which were correlated to RSV viral titre (quantitative PCR). Lung tissues were collected at 3, 5, 7 and 21 days post-infection (dpi) to assess leukocyte populations by flow cytometry. Clinical symptoms and RSV viral load peaked at 5 dpi. RSV-RFP was most prevalent in macrophages at 3 dpi and observed in B cells and DCs. At 21 dpi, RSV-RFP remained evident in a subset of conventional DCs (CD103 ⁺CD11b ⁺) even though clinical symptoms and pulmonary inflammation had resolved. This data indicates that RSV infects, replicates in and persists in a sub-population of lung cDCs after resolution of symptoms and clearance of virus from the airways. Understanding the implications of this adaptation is likely to provide crucial insights into the virus’s ability to generate annual epidemics of respiratory disease.