The SARS-CoV spike protein-mediated ACE2 down-regulation could contribute to the severity of lung pathologies such as pulmonary fibrosis and acute respiratory distress syndrome, since the counterbalance of ACE2 on angiotensin II production in the renin–angiotensin system is deregulated, affecting its ability to modulate the innate immune system and to regulate inflammation(19,25,26). This evidence concerns the gene ACE2 and acute respiratory distress syndrome.