Pathophysiology

Respiratory syncytial virus infects and destroys bronchiolar epithelial cells, leading to necrosis and sloughing of the epithelium. This disruption results in airway edema, increased mucus production, and bronchiolar obstruction.

Inflammatory cells like neutrophils and monocytes also infiltrate the peribronchial tissues, causing further airway narrowing. The partial obstruction and plugging of bronchioles causes air trapping, hyperinflation, and areas of collapsed alveoli in the lungs. This significantly impairs ventilation and gas exchange.

Additionally, RSV nonstructural proteins antagonize type I interferon signaling pathways, delaying the innate antiviral immune response.

Persistent inflammation may also impair neural control of airway smooth muscle, leading to airway hyperreactivity that persists after the infection clears.

Ultimately, severe RSV disease likely involves a combination of direct viral cytopathic effects on the bronchioles and dysregulated inflammatory host immune responses.