Human rhinoviruses are not only the main pathogens responsible for the common cold, but are now recognized to have a major impact on asthma pathogenesis. There is evidence that rhinovirus infections play a role in asthma development, asthma exacerbations and, potentially, airway remodeling. Children who experience repeated rhinovirus-induced wheezing episodes in infancy have a significantly increased risk of developing asthma, even when compared to children who experience wheezing induced by respiratory syncytial virus. Rhinovirus is also the dominant virus type associated with acute exacerbations of asthma. The epithelial cell is the principal site of rhinovirus infection in both the upper and lower airways and there is strong evidence that virus-induced alterations of epithelial cell biology play a critical role in regulating clinical outcomes. This includes rhinovirus-induced epithelial generation of a variety of chemokines, cytokines and growth factors that likely play a role in viral modulation of airway inflammation. It has also become clear, however, that epithelial cells play an important role in the innate antiviral response to rhinovirus infection, raising the possibility that the relative induction of epithelial host innate antiviral responses versus proinflammatory responses may be one factor regulating the susceptibility of asthmatic subjects to virus-induced disease exacerbations. Recent evidence has also highlighted that rhinovirus infection induces epithelial production of a number of growth factors and other mediators that could contribute to the development and progression of airway remodeling processes in asthma. The current article reviews our current state of knowledge in these areas.