Rhinovirus increases adhesion to the respiratory epithelium.

Rhinovirus causes many types of respiratory illnesses, ranging from minor colds to exacerbations of asthma. is an opportunistic pathogen that is increased in abundance during rhinovirus illnesses and asthma exacerbations and is associated with increased severity of illness through mechanisms that are ill-defined. We used a co-infection model of human airway epithelium differentiated at the air-liquid interface to test the hypothesis that rhinovirus infection promotes adhesion and survival on the respiratory epithelium. Initial experiments showed that infection with alone did not damage the epithelium or induce cytokine production, but increased trans-epithelial electrical resistance, indicative of increased barrier function. In a co-infection model, infection with the more virulent rhinovirus-A and rhinovirus-C, but not the less virulent rhinovirus-B types, increased cell-associated . Immunofluorescent staining demonstrated that adhered to rhinovirus-infected ciliated epithelial cells and infected cells being extruded from the epithelium. Rhinovirus induced pronounced changes in gene expression and secretion of inflammatory cytokines. In contrast, caused minimal effects and did not enhance RV-induced responses. Our results indicate that rhinovirus-A or C infection increases survival and cell association while infection alone does not cause cytopathology or epithelial inflammation. Our findings suggest that rhinovirus and co-infection could promote epithelial damage and more severe illness by amplifying leukocyte inflammatory responses at the epithelial surface.