Respiratory syncytial virus (RSV), a nonsegmented, single stranded RNA virus, infects one-half of all infants within the first year of life. RSV possesses pathogenetic qualities that may be attributed to the interplay of viral and host-specific factors including virus strains of different virulence, size of the inoculum, family history of asthma or airway hyperreactivity and immunologic anomalies of the host. Inflammatory cell recruitment and activation occur in response to RSV infection of epithelial cells. Epithelial cells initiate the inflammatory response to RSV by elaborating a wide variety of cytokines and chemokines that trigger further inflammatory responses. Helper T lymphocytes mediate the relative balance of cytokine production and also secrete a variety of antiviral and proinflammatory interleukins. Elevated levels of macrophage-inflammatory protein-1-alpha, an attractant of eosinophils, and monocyte chemotactic protein-1 parallel severe forms of bronchiolitis. Macrophage-inflammatory protein-1-alpha and monocyte chemotactic protein-1 levels also are inversely related to oxygen saturation, suggesting that severity of RSV disease may be linked to chemokine release. Children known to be eosinophilic during an episode of bronchiolitis appear more prone to wheeze at an older age. Influenza, parainfluenza and metapneumoviruses share major epidemiologic risk factors for lower respiratory tract infection similar to those of RSV. Like RSV some of these viruses may also promote an exaggerated lymphocyte-proliferative response, and subjects infected with parainfluenza viruses produce elevated levels of virus-specific IgE. Preliminary evidence suggests that severe RSV and influenza viral infections are mediated via chemokine up-regulation.