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Angiotensin-converting enzyme 2 (ACE2) and serine protease TMPRSS2 have been implicated in cell entry for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus responsible for coronavirus disease 2019 (COVID-19). The expression of  ACE2  and  TMPRSS2  in the lung epithelium might have implications for the risk of SARS-CoV-2 infection and severity of COVID-19. We use human genetic variants that proxy angiotensin-converting enzyme (ACE) inhibitor drug effects and cardiovascular risk factors to investigate whether these exposures affect lung  ACE2  and  TMPRSS2  gene expression and circulating ACE2 levels. We observed no consistent evidence of an association of genetically predicted serum ACE levels with any of our outcomes. There was weak evidence for an association of genetically predicted serum ACE levels with  ACE2  gene expression in the Lung eQTL Consortium ( p  = 0.014), but this finding did not replicate. There was evidence of a positive association of genetic liability to type 2 diabetes mellitus with lung  ACE2  gene expression in the Gene-Tissue Expression (GTEx) study ( p  = 4 × 10 −4 ) and with circulating plasma ACE2 levels in the INTERVAL study ( p  = 0.03), but not with lung  ACE2  expression in the Lung eQTL Consortium study ( p  = 0.68). There were no associations of genetically proxied liability to the other cardiometabolic traits with any outcome. This study does not provide consistent evidence to support an effect of serum ACE levels (as a proxy for ACE inhibitors) or cardiometabolic risk factors on lung  ACE2  and  TMPRSS2  expression or plasma ACE2 levels.

royal society open science

ACE inhibition and cardiometabolic risk factors, lung<i>ACE2</i>and<i>TMPRSS2</i>gene expression, and plasma ACE2 levels: a Mendelian randomization study

ACE inhibition and cardiometabolic risk factors, lungACE2andTMPRSS2gene expression, and plasma ACE2 levels: a Mendelian randomization study