About: Lack of association between genetic variants at ACE2 and TMPRSS2 genes involved in SARS-CoV-2 infection and human quantitative phenotypes

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About: Lack of association between genetic variants at ACE2 and TMPRSS2 genes involved in SARS-CoV-2 infection and human quantitative phenotypes Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Lack of association between genetic variants at ACE2 and TMPRSS2 genes involved in SARS-CoV-2 infection and human quantitative phenotypes
Creator	Swertz, Morris Sanna, Serena Deelen, Patrick Franke, Lude Fu, Jingyuan Lanting, Pauline Lopera, Esteban Study, Lifelines Van Der Geest, Marije Van Der Graaf, Adriaan Wijmenga, Cisca Zhernakova, Alexandra
Source	MedRxiv
abstract	Coronavirus disease 2019 (COVID-19) shows a wide variation in expression and severity of symptoms, from very mild or no symptomes, to flu-like symptoms, and in more severe cases, to pneumonia, acute respiratory distress syndrome and even death. Large differences in outcome have also been observed between males and females. The causes for this variability are likely to be multifactorial, and to include genetics. The SARS-CoV-2 virus responsible for the infection uses the human receptor angiotensin converting enzyme 2 (ACE2) for cell invasion, and the serine protease TMPRSS2 for S protein priming. Genetic variation in these two genes may thus modulate an individual's genetic predisposition to infection and virus clearance. While genetic data on COVID-19 patients is being gathered, we carried out a phenome-wide association scan (PheWAS) to investigate the role of these genes in other human phenotypes in the general population. We examined 178 quantitative phenotypes including cytokines and cardio-metabolic biomarkers, as well as 58 medications in 36,339 volunteers from the Lifelines population biobank, in relation to 1,273 genetic variants located in or near ACE2 and TMPRSS2. While none reached our threshold for significance, we observed a suggestive association of polymorphisms within the ACE2 gene with (1) the use of ARBs combination therapies (p=5.7x10-4), an association that is significantly stronger in females (pdiff=0.01), and (2) with the use of non-steroid anti-inflammatory and antirheumatic products (p=5.5x10-4). While these associations need to be confirmed in larger sample sizes, they suggest that these variants play a role in diseases such as hypertension and chronic inflammation that are often observed in the more severe COVID-19 cases. Further investigation of these genetic variants in the context of COVID-19 is thus promising for better understanding of disease variability. Full results are available at https://covid19research.nl.
has issue date	2020-04-25(xsd:dateTime)
bibo:doi	10.1101/2020.04.22.20074963
has license	medrxiv
sha1sum (hex)	216f37bd2a3833d9c90105a39175737ea5041a72
schema:url	https://doi.org/10.1101/2020.04.22.20074963
resource representing a document's title	Lack of association between genetic variants at ACE2 and TMPRSS2 genes involved in SARS-CoV-2 infection and human quantitative phenotypes
resource representing a document's body	covid:216f37bd2a3833d9c90105a39175737ea5041a72#body_text
is schema:about of	named entity 'COVID-19' named entity 'modulate' named entity 'cases' named entity 'While' named entity 'medications' named entity 'variation' named entity 'TMPRSS2' named entity 'ACE2' named entity 'PATIENTS' named entity 'DISEASES' named entity '178' named entity 'ANGIOTENSIN II RECEPTOR BLOCKERS' named entity 'BEING' named entity 'DEATH' named entity 'CAUSES' named entity 'INDIVIDUAL' named entity 'LARGER' named entity 'VARIABILITY' named entity 'CELL INVASION' named entity 'TMPRSS2' named entity 'METABOLIC' named entity 'PLAY' named entity '28P' named entity 'NEAR' named entity 'SEVERITY OF SYMPTOMS' named entity 'S PROTEIN' named entity 'ACE2' named entity 'MEDICATIONS' named entity 'carried' named entity 'TMPRSS2' named entity 'polymorphisms' named entity 'angiotensin' named entity 'COVID-19' named entity 'protein' named entity 'ACE2' named entity 'genetic variants' named entity 'genetic predisposition' named entity 'phenotypes' named entity 'ACE2' named entity 'hypertension' named entity 'ACE2' named entity 'gene' named entity 'serine protease' named entity 'genetic data' named entity 'angiotensin II receptor blockers' named entity 'biomarkers' named entity 'cytokines' named entity 'chronic inflammation' named entity 'Coronavirus disease 2019' named entity 'phenome' named entity 'COVID' named entity 'virus' named entity 'combination therapies' named entity 'TMPRSS2' named entity 'SARS-CoV-2' named entity 'TMPRSS2' named entity 'triglycerides' named entity 'genetic variants' named entity 'preprint' named entity 'TMPRSS2' named entity 'Helsinki Declaration' named entity 'COVID' named entity 'Rotterdam' named entity 'coughing' named entity 'adverse drug reaction' named entity 'NSAIDs' named entity 'SARS-CoV-2 virus' named entity 'potential treatments' named entity 'triglycerides' named entity 'statistical significance' named entity 'drug packaging' named entity 'odds ratio' named entity 'citrulline' named entity 'thrombocytes'

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