Lay summary
Coronavirus infections can lead to severe respiratory complications including pulmonary oedema. Impaired function of the epithelial Na+ channel (ENaC) in the lung is related to the formation of pulmonary oedema and evidence suggests that ENaC and viral proteins require identical host proteins (proteases) to be activated. We will explore the unknown role of ENaC in coronavirus infections and hypothesise that coronavirus hijacks host proteases causing a loss of ENaC function that contributes to the formation of pulmonary oedema. We will address our hypothesis by studying ENaC function in epithelial and endothelial cells of the lung in the absence and presence of virus proteins. We will further use new drugs aiming to restored ENaC function after exposure to virus proteins. Our study can identify a new, yet unknown target in coronavirus infectiousness and provide new opportunities for treatments for patients with coronavirus infections.