Respiratory syncytial virus (RSV) is predominantly recognized as a pediatric pathogen although sensitive molecular diagnostic techniques have led to its more frequent detection in some adult settings. In some studies RSV has been detected just as frequently in stable chronic obstructive pulmonary disease (COPD) patients as in those suffering disease exacerbations, leading to the suggestion that RSV may persist in COPD. Although some studies have found negligible RSV in stable COPD, others have detected RSV in one-quarter to one-third of stable COPD samples. Possible reasons for this discrepancy are explored within the article. A relationship between RSV detection and increased disease severity, including rate of decline in lung function and systemic/airway inflammation, has been found on both occasions it has been sought. Susceptibility to persistent RSV infection could involve both host and viral factors. Cigarette smoking and COPD are likely to result in impaired antiviral immunity, and RSV is capable of evading immune responses by inducing skewed type 2 T-helper cell responses, antagonizing antiviral cytokines, mimicking chemokines, inhibiting apoptosis, and entering immune-privileged cells such as pulmonary neurons. It can also escape an established immune response through antigenic drift. This article examines current evidence regarding persistence of RSV in COPD and its possible mechanisms. We also discuss various roles for RSV persistence in COPD pathogenesis. Further elucidation of the contribution of persistent RSV to the pathogenesis of COPD requires interventional studies. Persistence of RSV in COPD may have direct relevance to the pathogenesis of childhood diseases such as postbronchiolitic wheeze and asthma.