RSV infects bronchiolar epithelial cells via fusion protein-mediated entry, causing necrosis, ciliary destruction, peribronchiolar lymphocytic infiltration, submucosal edema, and mucus hypersecretion. In infants, bronchiolar lumens are less than 1 mm; even 1 mm of circumferential edema reduces cross-sectional area by approximately 75%. A ball-valve mechanism develops where air enters on inspiration but becomes trapped on expiration, causing hyperinflation, air trapping, ventilation-perfusion mismatch, and hypoxemia. The immature infant immune response produces an exaggerated inflammatory reaction with neutrophil and eosinophil recruitment, worsening airway obstruction.