Impact of ACE I gene insertion/deletion, A-240T polymorphisms and the renin–angiotensin–aldosterone system on COVID-19 disease
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Published:2024-01-10
Issue:1
Volume:21
Page:
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ISSN:1743-422X
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Container-title:Virology Journal
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language:en
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Short-container-title:Virol J
Author:
Zobel Christian M.ORCID, Kuhn HartmutORCID, Schreiner MaximilianORCID, Wenzel WernerORCID, Wendtland JasperORCID, Goekeri CengizORCID, Scheit LorenzORCID, Oltmanns Klaas, Rauschning DominicORCID, Grossegesse MaricaORCID, Hofmann Natalie, Wirtz HubertORCID, Spethmann SebastianORCID, Baumgarten Ullrich, Wageloehner Tobias, Neumann Nino, Mueller Annette, Mueller Rico, Krueger Jan Philip, Borchert Alena, Weinreich Felix, Keidel Franziska, Koch Maria, Schüßler Meike,
Abstract
Abstract
Background
The coronavirus disease 2019 (COVID-19) pandemic is driven by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, which has led to an enormous burden on patient morbidity and mortality. The renin–angiotensin–aldosterone system (RAAS) plays a significant role in various pulmonary diseases. Since SARS-CoV-2 utilizes the angiotensin-converting enzyme (ACE)2 receptor to exert its virulence and pathogenicity, the RAAS is of particular importance in COVID 19.
Methods
Our preliminary study investigates retrospectively the influence of selected ACE-polymorphisms (I/D location at intron 16 in the B-coding sequence (rs4646994) and A-240T (rs 4291) at the A-promoter) as well as ACE1 and ACE2 serum levels on disease severity and the inflammatory response in inpatients and outpatients with COVID-19.
Results
Our study included 96 outpatients and 88 inpatients (65.9% male, mean age 60 years) with COVID-19 from April to December 2020 in four locations in Germany. Of the hospitalized patients, 88.6% participants were moderately ill (n = 78, 64% male, median age 60 years), and 11.4% participants were severely ill or deceased (n = 10, 90% male, median age 71 years). We found no polymorphism-related difference in disease, in age distribution, time to hospitalization and time of hospitalization for the inpatient group. ACE1 serum levels were significantly increased in the DD compared to the II polymorphism and in the TT compared to the AA polymorphism. There was no significant difference in ACE 1 serum levels l between moderately ill and severely ill patients. However, participants requiring oxygen supplementation had significantly elevated ACE1 levels compared to participants not requiring oxygen, with no difference in ACE2 levels whereas females had significantly higher ACE2 levels.
Conclusions
Although there were no differences in the distribution of ACE polymorphisms in disease severity, we found increased proinflammatory regulation of the RAAS in patients with oxygen demand and increased serum ACE2 levels in women, indicating a possible enhanced anti-inflammatory immune response.
Clinical trial registration: PreBiSeCov: German Clinical Trials Register, DRKS-ID: DRKS00021591, Registered on 27th April 2020.
Funder
Sanitätsakademie der Bundeswehr, Abteilung E
Publisher
Springer Science and Business Media LLC
Subject
Infectious Diseases,Virology
Reference42 articles.
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