Abstract

COVID-19 has led to morbidity in millions of patients, ranging from mild flu-like symptoms to severe respiratory failure, necessitating oxygen supplementation and mechanical ventilation, and ultimately death. The SARS-CoV-2 virus reacts with angiotensin-converting enzyme 2 (ACE2) molecules that are especially found in alveolar epithelial type 2 cells in the lungs and thereby causes a loss in lung surfactant, a protein-lipid mixture that is crucial for both native immunity and reduction of surface tension in the lung alveoli. Lung surfactant insufficiency results in atelectasis and loss of functional lung tissue amid an inflammatory storm and may be countered by treating COVID-19 pneumonia patients with exogenous lung surfactant, preferably by aerosol delivery of a novel dry powder synthetic lung surfactant. More research on timing, dosing, and delivery of synthetic lung surfactant in patients with COVID-19 pneumonia is of crucial importance to implement this approach in clinical practice.

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