Viral respiratory tract infections are associated with an acute increase in airway responsiveness in normal subjects and patients with asthma. Airway responsiveness is also increased at least transiently in animals during acute viral infections. In this article, we discuss possible mechanisms whereby viral infections can increase airway responsiveness, emphasizing the effects of viral-induced airway epithelial damage during acute lytic infection and the mechanical consequences of airway inflammation and edema, both internal and external to the smooth muscle layer. We also describe possible mechanisms by which acute lytic viral infections could induce chronic sequelae in atopic individuals and contribute to the development of persistence of asthma. Finally, results of recent studies from our laboratory that document adenoviral genome in lungs of patients with chronic obstructive pulmonary disease (COPD) and long-term persistence of respiratory syncytial viral genome and protein in an animal model are discussed in terms of the possible role of latent and persistent viral infections in the pathogenesis of asthma and COPD.