Abstract Rationale Rhinovirus (RV) infections can alter lower airway physiology, yet the characteristics of RV replication in lower airway cells and their relationship to inflammation are incompletely understood. We hypothesized that RV infections extend to the lower airway and may persist for over a week. Methods To test this hypothesis, bronchoscopy with bronchial biopsies and brushings was performed 4 and 15 days after nasal inoculation of 11 subjects (4 normal and 7 with allergic asthma) with RV16. Samples were paraffin-embedded, sectioned and then stained with a monoclonal antibody against RV16. Results All subjects had clinical colds confirmed by titration of virus from nasal lavages. None of the bronchial samples taken from subjects pre-inoculation had any positively-staining cells. Post inoculation, virus was detected by staining in 9 of 11 subjects, and in 39 and 48% of the samples taken after 4 and 15 days, respectively. Infected epithelial cells were distributed in discrete patches and were typically present in only one or two out of 4 to 5 available biopsy samples obtained during the acute cold. There were no significant differences between normal and asthmatic subjects. Conclusions These results confirm that the lower airway is infected during the acute and convalescent cold, with a patchy distribution of infected cells, similar to that reported in upper airway tissues. Extension of RV into lower airways could be one mechanism responsible for pulmonary symptoms and altered respiratory physiology seen in susceptible individuals.