IFNβ1 seems to be a significant IFN-I in the treatment of Coronavirus infections due to its protective activity in lung through upregulating cluster differentiation 73 (CD73) in lung endothelial cells, inducing secretion of adenosine as an anti-inflammatory agent, and inducing discretion of vascular leakage in acute respiratory distress syndrome (ARDS) (62, 63). This evidence concerns the gene NT5E and acute respiratory distress syndrome.