Abstract
Cystic fibrosis (CF) is one of the most common autosomal recessive life-limiting conditions affecting Caucasians. The resulting defect in the cystic fibrosis transmembrane conductance regulator protein (CFTR) results in defective chloride and bicarbonate secretion, as well as dysregulation of epithelial sodium channels (ENaC). These changes bring about defective mucociliary clearance, reduced airway surface liquid and an exaggerated proinflammatory response driven, in part, by infection. In this short article we explore the overlap in the pathophysiology of CF and COVID-19 infection and discuss how understanding the interaction between both diseases may shed light on future treatments.
MeSH terms
-
Angiotensin-Converting Enzyme 2
-
Animals
-
COVID-19
-
Coronavirus Infections / complications
-
Coronavirus Infections / drug therapy
-
Coronavirus Infections / metabolism*
-
Coronavirus Infections / virology
-
Cystic Fibrosis / complications
-
Cystic Fibrosis / drug therapy
-
Cystic Fibrosis / metabolism*
-
Cystic Fibrosis Transmembrane Conductance Regulator / metabolism
-
Cytokines / metabolism
-
Humans
-
Pandemics
-
Peptidyl-Dipeptidase A / metabolism
-
Pneumonia, Viral / complications
-
Pneumonia, Viral / drug therapy
-
Pneumonia, Viral / metabolism*
-
Pneumonia, Viral / virology
Substances
-
Cytokines
-
Cystic Fibrosis Transmembrane Conductance Regulator
-
Peptidyl-Dipeptidase A
-
ACE2 protein, human
-
Angiotensin-Converting Enzyme 2