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Möhlendick, Birte; Schönfelder, Kristina; Breuckmann, Katharina; Elsner, Carina; Babel, Nina; Balfanz, Paul; Dahl, Edgar; Dreher, Michael; Fistera, David; Herbstreit, Frank; Hölzer, Bodo; Koch, Michael; Kohnle, Matthias; Marx, Nikolaus; Risse, Joachim; Schmidt, Karsten; Skrzypczyk, Sarah; Sutharsan, Sivagurunathan; Taube, Christian; Westhoff, Timm H.; Jöckel, Karl-Heinz; Dittmer, Ulf; Siffert, Winfried; Kribben, Andreas

ACE2 polymorphism and susceptibility for SARS-CoV-2 infection and severity of COVID-19

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  • Medientyp: E-Artikel
  • Titel: ACE2 polymorphism and susceptibility for SARS-CoV-2 infection and severity of COVID-19
  • Beteiligte: Möhlendick, Birte; Schönfelder, Kristina; Breuckmann, Katharina; Elsner, Carina; Babel, Nina; Balfanz, Paul; Dahl, Edgar; Dreher, Michael; Fistera, David; Herbstreit, Frank; Hölzer, Bodo; Koch, Michael; Kohnle, Matthias; Marx, Nikolaus; Risse, Joachim; Schmidt, Karsten; Skrzypczyk, Sarah; Sutharsan, Sivagurunathan; Taube, Christian; Westhoff, Timm H.; Jöckel, Karl-Heinz; Dittmer, Ulf; Siffert, Winfried; Kribben, Andreas
  • Erschienen: Ovid Technologies (Wolters Kluwer Health), 2021
  • Erschienen in: Pharmacogenetics and Genomics
  • Sprache: Englisch
  • DOI: 10.1097/fpc.0000000000000436
  • ISSN: 1744-6872
  • Schlagwörter: Genetics (clinical) ; Genetics ; Molecular Biology ; Molecular Medicine ; General Pharmacology, Toxicology and Pharmaceutics
  • Entstehung:
  • Anmerkungen:
  • Beschreibung: <jats:sec> <jats:title>Objectives</jats:title> <jats:p>The RNA virus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is responsible for coronavirus disease 2019 (COVID-19). Cell entry is mediated by the human angiotensin-converting enzyme II (ACE2). <jats:italic toggle="yes">ACE2</jats:italic> and its close homolog angiotensin-converting enzyme I (<jats:italic toggle="yes">ACE</jats:italic>) are currently discussed candidate genes, in which single-nucleotide polymorphisms (SNPs) could alter binding or entry of SARS-CoV-2 and enhance tissue damage in the lung or other organs. This could increase the susceptibility for SARS-CoV-2 infection and the severity of COVID-19.</jats:p> </jats:sec> <jats:sec> <jats:title>Patients and methods</jats:title> <jats:p>We performed genotyping of SNPs in the genes <jats:italic toggle="yes">ACE2</jats:italic> and <jats:italic toggle="yes">ACE</jats:italic> in 297 SARS-CoV-2-positive and 253 SARS-CoV-2-negative tested patients. We analyzed the association of the SNPs with susceptibility for SARS-CoV-2 infection and the severity of COVID-19.</jats:p> </jats:sec> <jats:sec> <jats:title>Results</jats:title> <jats:p>SARS-CoV-2-positive and SARS-CoV-2-negative patients did not differ regarding demographics and clinical characteristics. For <jats:italic toggle="yes">ACE2</jats:italic> rs2285666, the GG genotype or G-allele was significantly associated with an almost two-fold increased SARS-CoV-2 infection risk and a three-fold increased risk to develop serious disease or COVID-19 fatality. In contrast, the <jats:italic toggle="yes">ACE</jats:italic> polymorphism was not related to infection risk or severity of disease. In a multivariable analysis, the <jats:italic toggle="yes">ACE2</jats:italic> rs2285666 G-allele remained as an independent risk factor for serious disease besides the known risk factors male gender and cardiovascular disease.</jats:p> </jats:sec> <jats:sec> <jats:title>Conclusions</jats:title> <jats:p>In summary, our report appears to be the first showing that a common <jats:italic toggle="yes">ACE2</jats:italic> polymorphism impacts the risk for SARS-CoV-2 infection and the course of COVID-19 independently from previously described risk factors.</jats:p> </jats:sec>