{"doi":"10.1101/2020.05.05.20075507","title":"Clinical and Genetic Characteristics of Covid-19 Patients from UK Biobank","abstract":"Abstract Objective To explore both clinical and genetic risk factors for Covid-19 in a cohort from the United Kingdom. Design Prospective cohort study. Participants 669 positive Covid-19 patients within a cohort of 502,536 UK Biobank participants, recruited between 2006 and 2010. Main Outcome Measures The main outcome measure was Covid-19 positive status, determined by the presence of any positive test for a single individual. We also assessed risk factors for inpatient and outpatient status for Covid-19 positive individuals. Results We found that black participants were at over three times increased risk of testing positive for Covid-19, relative to white participants, even after adjusting for confounders (adjusted relative risk [ARR] 3.14, 95% confidence interval [CI] 2.28 to 4.31). Asian participants were also at higher risk of Covid-19 (ARR 2.03, 95% CI 1.40 to 2.95). Next, we analyzed the association of comorbidities with Covid-19. We found that participants were at increased risk of Covid-19 if they had chronic obstructive pulmonary disease (ARR 1.54, 95% CI 1.02 to 2.31) or ischemic heart disease (ARR 1.56, 95% CI 1.18 to 2.07). However, there was no evidence that either angiotensin converting enzyme inhibitors (ARR 1.32, 95% CI 0.95 to 1.84) or angiotensin II receptor blockers (ARR 1.37, 95% CI 0.94 to 1.98) increased the risk of Covid-19. We confirmed that blood type A was associated with Covid-19 relative to blood type O individuals, and we also found that the HLA variant DQA1_509 was enriched in Covid-19 positive cases, even after Bonferroni correction (P = 1.0 x 10 −5 ). Conclusions In this study, we found that black and Asian participants were at increased risk of Covid-19, even after adjusting for confounders. We also identified a novel genetic association with the HLA variant DQA1_509. Further investigations of genetic associations with Covid-19 may lead to important discoveries of genetic drivers of severe disease.","journal":"medRxiv","year":2020,"id":118911,"datarank":1.952289528808691,"base_score":3.58351893845611,"endowment":3.58351893845611,"self_citation_contribution":0.5375278407684165,"citation_network_contribution":1.4147616880402745,"self_endowment_contribution":0.5375278407684165,"citer_contribution":1.4147616880402745,"corpus_percentile":89.11580413088883,"corpus_rank":1408,"citation_count":35,"citer_count":35,"citers_with_citation_signal":32,"citers_with_endowment":32,"datacite_reuse_total":0,"is_dataset":true,"is_dataset_confidence":0.5767,"is_data_producer":false,"deposit_databanks":null,"is_oa":true,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":"2020-01-01","fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":321209,"name":"Scott Kulm","orcid":"0000-0003-2156-1459","position":1,"is_corresponding":false},{"id":41043,"name":"Olivier Elemento","orcid":"0000-0002-8061-9617","position":2,"is_corresponding":false},{"id":321208,"name":"David A. Kolin","orcid":"0000-0002-5306-023X","position":0,"is_corresponding":true}],"reference_count":12,"raw_metadata":null,"created_at":"2026-07-18T23:14:03.409507Z","pmid":"32511589","pmcid":"PMC7276016","fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}