Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus that causes the disease covid-19, is characterized by high mortality among the elderly. The main manifestation that separates this virus from other beta-coronaviruses, is associated with the increased risk of pneumonia, that leads to acute respiratory distress syndrome (ARDS). Any tissue damage in the periphery, is triggered by the excess of cytokines, that are released in the bloodstream, after the initiation of ARDS. Moreover, the virus appears to have the RNAemia trait, a condition that is also witnessed in the case of the human immunodeficiency virus (HIV), but the difference lies in the inability of the former to be transmitted through blood. The angiotensin-converting enzyme 2 receptor (ACE2R) downregulation leads to increased renin-angiotensin system (RAS) activation, and also decreased activity of the Mas receptor, a well-known GPCR, which is the substrate for the ligand angiotensin 1-7, which is produced by the conversion of angiotensin II, by the ACE2R. Last but not least, since pneumonia is one of the main causes of acute lung injury (ALI), the latter, present due to severe damage to the main pulmonary artery, we hence claim that medication used for the treatment of pulmonary hypertension could decrease the fatality risk of pneumonia, and in combination with the standard approach of corticosteroids, antiviral agents, and NO administration, could alleviate, or even eradicate pneumonia symptoms.