Respiratory syncytial virus (RSV), named by its ability to induce fusion of infected epithelial cells (49), is a leading cause of epidemic respiratory tract illness in children (28). Spread primarily by contact with contaminated secretions, RSV replicates in the nasopharyngeal epithelium and spreads to the lower respiratory tract via epithelial cell-to-cell transfer along intracytoplasmic bridges (27). Although only two RSV serotypes, A and B, circulate in RSV epidemics (29), immunity to naturally acquired infection is incomplete, resulting in repeated infections through adulthood (24; reviewed in reference 28). In humans, RSV infection produces a spectrum of airway involvement ranging from otitis media to lower tract infection.Clinically severe RSV infections involving the lower respiratory tract are primarily seen in young children with naïve immune systems and/or genetic predispositions (32), patients with suppressed T-cell immunity (such as heart transplant recipients [41]), and the elderly (48). In autopsy studies of fatal disease, RSV infection is characterized by the presence of cytoplasmic eosinophilic inclusion bodies, characteristic of viral replication, in airway epithelial cells; sloughing and necrosis of the epithelial surface; and concomitant mucous plugging of the airways with trapping of air (1,18,19). In addition to these manifestations of direct epithelial involvement, RSV infection produces a pronounced perivascular infiltrate of mononuclear cells and lymphocytes (1, 18) and a neutrophil-rich exudate detected by bronchoalveolar lavage (16). Finally, the presence of eosinophil cationic protein (20,30) and histamine (64) in nasal secretions at concentrations that correlate with disease severity suggests the participation of eosinophils and basophils in the pathology of RSV infection.The mechanisms responsible for recruitment of circulating leukocytes, mononuclear cells, and lymphocytes into the lung as a consequence of RSV infection are largely unknown. Cellular recruitment into inflamed tissues is a multistep process in which circulating leukocytes first demarginate, adhere to stimulated endothelial cells, and subsequently become activated. Activated leukocytes then migrate through the vascular endothelium toward chemical gradients of chemoattractant peptides or antigens (reviewed in reference 58). Recent attention has focused on the important role of chemokines in mediat-* Corresponding author. Mailing address: Division of Endocrinology, MRB 8.138, The University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555-1060.