Abstract
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.
Original language | English (US) |
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Pages (from-to) | 695-703 |
Number of pages | 9 |
Journal | Pharmacogenomics |
Volume | 21 |
Issue number | 10 |
DOIs | |
State | Published - Jul 2020 |
Keywords
- ACE-inhibition
- ACE2
- COVID-19
- angiotensin-receptor blockade
- angiotensinogen
- cardiac dysfunction
- coronavirus
- genomics
- renin
- respiratory failure
ASJC Scopus subject areas
- Molecular Medicine
- Genetics
- Pharmacology