ACE2 and COVID-19: using antihypertensive medications and pharmacogenetic considerations.
COVID-19 utilizes the ACE2 pathway as a means of infection. Early data on COVID-19 suggest heterogeneity in the severity of symptoms during transmission and infection ranging from no symptoms to death. The source of this heterogeneity is likely multifaceted and may have a genetic component. Demographic and clinical comorbidities associated with the severity of infection suggest that possible variants known to influence the renin-angiotensin-aldosterone (RAAS) system pathway (particularly those that influence ACE2) may contribute to the heterogenous infection response. ACE2 and Ang(1-7) (the product of ACE2) seem to have a protective effect on the pulmonary and cardiac systems. Hypertension medication modulation, may alter ACE2 and Ang(1-7), particularly in variants that have been shown to influence RAAS system function, which could be clinically useful in patients with COVID-19.
['Snyder|Eric M|EM|', 'Johnson|Bruce D|BD|']
D047228:Angiotensin II Type 1 Receptor Blockers D000085962:Angiotensin-Converting Enzyme 2 D000959:Antihypertensive Agents D000086382:COVID-19 D018352:Coronavirus Infections D006801:Humans D058873:Pandemics D007703:Peptidyl-Dipeptidase A D010597:Pharmacogenetics D000071185:Pharmacogenomic Testing D011024:Pneumonia, Viral D012084:Renin-Angiotensin System
ACE2 COVID-19 ACE-inhibition angiotensin-receptor blockade angiotensinogen cardiac dysfunction coronavirus genomics renin respiratory failure