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 : wasabi.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	Hoffmann, Markus Swertz, Morris Sanna, Serena Deelen, Patrick Franke, Lude Fu, Jingyuan Lanting, Pauline Study, Lifelines Van Der Geest, Marije Van Der Graaf, Adriaan Wijmenga, Cisca Zhernakova, Alexandra Kaakinen, Marika Kuiper, Jonas Lopera Maya, Esteban Maya, Lopera
Source	Medline; PMC; WHO
abstract	Coronavirus disease 2019 (COVID-19) shows a wide variation in expression and severity of symptoms, from very mild or no symptoms, 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 depends on two human genes: 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 usage of 58 medications in 36,339 volunteers from the Lifelines population cohort, in relation to 1,273 genetic variants located in or near ACE2 and TMPRSS2. While none reached our threshold for significance, we observed several interesting suggestive associations. For example, single nucleotide polymorphisms (SNPs) near the TMPRSS2 genes were associated with thrombocytes count (p = 1.8 × 10(−5)). SNPs within the ACE2 gene were associated with (1) the use of angiotensin II receptor blockers (ARBs) combination therapies (p = 5.7 × 10(−4)), an association that is significantly stronger in females (p(dif)(f) = 0.01), and (2) with the use of non-steroid anti-inflammatory and antirheumatic products (p = 5.5 × 10(−4)). While these associations need to be confirmed in larger sample sizes, they suggest that these variants could play a role in diseases such as thrombocytopenia, 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	2020-06-08(xsd:dateTime)
bibo:doi	10.3389/fgene.2020.00613
bibo:pmid	32582302
has license	cc-by
sha1sum (hex)	f5d6aa2b152f99927df54c9e0de0867c029ef66c
schema:url	https://doi.org/10.3389/fgene.2020.00613
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
has PubMed Central identifier	PMC7295011
has PubMed identifier	32582302
schema:publication	Front Genet
resource representing a document's body	covid:f5d6aa2b152f99927df54c9e0de0867c029ef66c#body_text
is schema:about of	named entity 'investigate' named entity 'relation' named entity 'females' named entity 'flu-like symptoms' named entity 'threshold' named entity 'Phenotypes' named entity 'INTERESTING' named entity 'OUR' named entity 'VOLUNTEERS' named entity '28P' named entity 'THROMBOCYTES' named entity 'VIRUS CLEARANCE' named entity 'FEMALES' named entity 'DIF' named entity 'NON-' named entity 'CELL INVASION' named entity 'COVID-19' named entity 'MALES' named entity '5.7' named entity 'CORONAVIRUS DISEASE 2019' named entity 'blockers' named entity 'individual' named entity 'The' named entity 'priming' named entity 'angiotensin' named entity 'associations' named entity 'ACE2' named entity 'TMPRSS2' named entity 'symptoms' named entity 'COVID-19' named entity 'While' named entity 'receptor' named entity 'phenotypes' named entity 'Variants' named entity 'protein' named entity 'ACE2' named entity 'infection' named entity 'antirheumatic' named entity 'ACE2' named entity 'cytokines' named entity 'anti-inflammatory' named entity 'non-steroid' named entity 'angiotensin II receptor blockers' named entity '0.01' named entity 'genetic predisposition' named entity 'TMPRSS2' named entity 'suggestive' named entity 'Statistical power' named entity 'general population' named entity 'odds ratio' named entity 'minor allele frequency' named entity 'TMPRSS2' named entity 'COVID' named entity 'SARS-CoV-2' named entity 'coughing' named entity 'beta-thalassemia' named entity 'drug usage' named entity 'TMPRSS2' named entity 'fever' named entity 'host cell' named entity 'COVID-19' named entity 'immunoassay' named entity 'Sweden' named entity 'chronic inflammation' named entity 'physiological processes' named entity 'ACE2'

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