<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Cappadona C</submitter><funding>Banca Intesa San Paolo</funding><pagination>1166</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8622845</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>11(11)</volume><pubmed_abstract>Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the etiologic agent of the coronavirus disease 2019 (COVID-19) pandemic. Besides virus intrinsic characteristics, the host genetic makeup is predicted to account for the extreme clinical heterogeneity of the disease, which is characterized, among other manifestations, by a derangement of hemostasis associated with thromboembolic events. To date, large-scale studies confirmed that genetic predisposition plays a role in COVID-19 severity, pinpointing several susceptibility genes, often characterized by immunologic functions. With these premises, we performed an association study of common variants in 32 hemostatic genes with COVID-19 severity. We investigated 49,845 single-nucleotide polymorphism in a cohort of 332 Italian sever</pubmed_abstract><journal>Journal of personalized medicine</journal><pubmed_title>MEDTEC Students against Coronavirus: Investigating the Role of Hemostatic Genes in the Predisposition to COVID-19 Severity.</pubmed_title><pmcid>PMC8622845</pmcid><funding_grant_id>-</funding_grant_id><pubmed_authors>Gerussi A</pubmed_authors><pubmed_authors>D'Eugenio D</pubmed_authors><pubmed_authors>Corbella P</pubmed_authors><pubmed_authors>Papatolo A</pubmed_authors><pubmed_authors>Carloni F</pubmed_authors><pubmed_authors>Cameroni C</pubmed_authors><pubmed_authors>Guerrera L</pubmed_authors><pubmed_authors>Ziliotto N</pubmed_authors><pubmed_authors>Lopedote L</pubmed_authors><pubmed_authors>Franke A</pubmed_authors><pubmed_authors>Grondelli MC</pubmed_authors><pubmed_authors>Menga LM</pubmed_authors><pubmed_authors>Dal Ri G</pubmed_authors><pubmed_authors>Smidili A</pubmed_authors><pubmed_authors>Tartaglia FC</pubmed_authors><pubmed_authors>Asselta R</pubmed_authors><pubmed_authors>Duga S</pubmed_authors><pubmed_authors>Mariola C</pubmed_authors><pubmed_authors>Montorsi G</pubmed_authors><pubmed_authors>Bolchini C</pubmed_authors><pubmed_authors>Cappadona C</pubmed_authors><pubmed_authors>Rimoldi V</pubmed_authors><pubmed_authors>Invernizzi P</pubmed_authors><pubmed_authors>Di Giorgio SM</pubmed_authors><pubmed_authors>Degenhardt F</pubmed_authors><pubmed_authors>Bottaro S</pubmed_authors><pubmed_authors>Composto A</pubmed_authors><pubmed_authors>Matronola GM</pubmed_authors><pubmed_authors>Cavadini G</pubmed_authors><pubmed_authors>Brenna D</pubmed_authors><pubmed_authors>Converso G</pubmed_authors><pubmed_authors>Azimonti A</pubmed_authors><pubmed_authors>Paraboschi EM</pubmed_authors><pubmed_authors>Campanaro G</pubmed_authors><pubmed_authors>Marconi E</pubmed_authors><pubmed_authors>Brunati A</pubmed_authors><pubmed_authors>Pattini L</pubmed_authors><pubmed_authors>Laffoucriere G</pubmed_authors><pubmed_authors>Tettamanzi G</pubmed_authors><pubmed_authors>Profeta L</pubmed_authors><pubmed_authors>Rebasti V</pubmed_authors><pubmed_authors>Tinelli E</pubmed_authors><pubmed_authors>Lando B</pubmed_authors><pubmed_authors>Patti R</pubmed_authors><pubmed_authors>Maizza B</pubmed_authors><pubmed_authors>Tarchi SM</pubmed_authors><pubmed_authors>Ciravegna M</pubmed_authors><pubmed_authors>Stuani R</pubmed_authors></additional><is_claimable>false</is_claimable><name>MEDTEC Students against Coronavirus: Investigating the Role of Hemostatic Genes in the Predisposition to COVID-19 Severity.</name><description>Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the etiologic agent of the coronavirus disease 2019 (COVID-19) pandemic. Besides virus intrinsic characteristics, the host genetic makeup is predicted to account for the extreme clinical heterogeneity of the disease, which is characterized, among other manifestations, by a derangement of hemostasis associated with thromboembolic events. To date, large-scale studies confirmed that genetic predisposition plays a role in COVID-19 severity, pinpointing several susceptibility genes, often characterized by immunologic functions. With these premises, we performed an association study of common variants in 32 hemostatic genes with COVID-19 severity. We investigated 49,845 single-nucleotide polymorphism in a cohort of 332 Italian sever</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Nov</publication><modification>2025-04-04T11:13:37.25Z</modification><creation>2022-02-11T13:35:05.247Z</creation></dates><accession>S-EPMC8622845</accession><cross_references><pubmed>34834519</pubmed><doi>10.3390/jpm11111166</doi></cross_references></HashMap>