Several symptoms of COVID-19 in the lungs, including severe mucus production, poor airway self-cleaning, and thickening of the bronchial wall, closely resemble those seen in people with cystic fibrosis. Genetic cystic fibrosis is caused by a defective or missing CFTR protein (CFTR: cystic fibrosis transmembrane conductance regulator). Covid-19 could be considered “acquired CTFR dysfunction” because the Covid-19 virus affects the immune system in a way that down-regulates the formation of CTFR protein in the lungs. Researchers at the University of Toronto have scientifically investigated these connections. They now suggest that CFTR drugs, which have been shown to be effective, may also be beneficial for COVID-19 patients by restoring CFTR expression. A further benefit is that CFTR therapeutics have anti-inflammatory properties that dampen exaggerated immune responses, while promoting cerebral vasodilatation. This aspect may provide some protection against COVID-19-related strokes.

Since CFTR therapeutics are currently only approved for treatment of cystic fibrosis, clinical trials demonstrating efficacy in COVID-19 treatment must now follow.