{"doi":"10.1111/bjh.16984","title":"ABO phenotype and death in critically ill patients with COVID‐19","abstract":"Blood groups are inherited traits that vary across populations, likely due to both founder effects and natural selection.1 A link between blood groups and susceptibility to infectious disease has been well-described, with notable examples being H. Pylori and Plasmodium falciparum infection.1, 2 Blood group antigens may influence disease susceptibility by several mechanisms, including serving as receptors or decoys for infectious organisms and modifying immune response in the form of anti-ABO antibodies.2 Data on the relationship between blood group and outcomes in patients with coronavirus disease 2019 (COVID-19) are limited. Studies from China3 and Europe4 reported that patients with type O blood may be protected from COVID-19 infection, whereas those with type A blood may be at higher risk. Data from a related viral outbreak, the severe acute respiratory syndrome coronavirus (SARS-CoV-1) in 2003, suggested that healthcare workers with type O blood were less likely to contract this disease.5 In vitro experiments revealed that the interaction between the SARS-CoV-1 spike protein and angiotensin converting enzyme 2 (ACE2), necessary for viral uptake, may be mitigated by anti-A antibodies.6 To examine the relationship between blood group and clinical outcomes in patients with COVID-19, we studied the distribution and mortality associated with ABO phenotype in a large cohort of critically ill patients. We utilised data from the Study of the Treatment and Outcomes in critically ill Patients with COVID-19 (STOP-COVID), a multicentre cohort study that enrolled consecutive adults (aged ≥18 years) with laboratory confirmed COVID-19 admitted to participating intensive care units (ICUs) at 67 hospitals across the United States. We included patients admitted to ICUs between 4 March and 11 April 2020. We followed patients until the first of hospital discharge, death or 8 May 2020, the date on which the database for the present analysis was locked. All patients who remained hospitalised at the time of analysis had a minimum of 28-days follow-up. The study was approved with a waiver of informed consent by the Institutional Review Board at each participating site. To examine whether blood type is associated with critical illness in patients with COVID-19, we used a chi-square test to compare the observed versus expected distribution of ABO phenotypes. We stratified our analyses by race/ethnicity, as race/ethnicity is an important determinant of ABO phenotype7 and could also affect hospitalisation for COVID-19. To improve the reliability of our estimates, we limited our analyses to the three most commonly reported categories of race/ethnicity in our cohort: white non-Hispanic; Black non-Hispanic; and Hispanic. Patients missing data on ABO phenotype were excluded. We estimated the expected distribution of ABO phenotype in each of the above race/ethnicity categories using data from 3·1 million blood donors in the United States.7 To examine whether ABO phenotype is associated with mortality among critically ill patients with COVID-19, we used a chi-square test to compare the distribution of observed ABO blood phenotypes with 28-day in-hospital mortality, stratified by the above race/ethnicity categories. Patients discharged alive from the hospital prior to 28 days were considered to be alive at 28 days. We tested the validity of this assumption in a random subset of 50 patients discharged prior to 28 days, all of whom remained alive at 28 days according to electronic medical records or follow-up by telephone. Statistical analysis was performed using GraphPad Prism 7 (GraphPad, Inc., San Diego, CA, USA), and Microsoft Excel 2016 (Microsoft Corp., Redmond, WA, USA). Among 3239 critically ill patients with COVID-19, 2033 (62·8%) had data available on ABO phenotype and were included in the present analysis. The median (interquartile range) age was 62 (52–71) years, and 1297 (63·8%) were men. Additional characteristics according to ABO phenotype are ","journal":"British Journal of Haematology","year":2020,"id":57002,"datarank":0.0,"base_score":0.0,"endowment":0.0,"self_citation_contribution":0.0,"citation_network_contribution":0.0,"self_endowment_contribution":0.0,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":81,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.9674,"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":140236,"name":"Hanny Al-Samkari","orcid":"0000-0001-6175-1383","position":1,"is_corresponding":false},{"id":243753,"name":"Samantha K. Brenner","orcid":null,"position":2,"is_corresponding":false},{"id":108943,"name":"Shruti Gupta","orcid":"0000-0002-5747-2151","position":3,"is_corresponding":false},{"id":140241,"name":"David E. Leaf","orcid":"0000-0001-7875-090X","position":4,"is_corresponding":false},{"id":297357,"name":"Rebecca Karp Leaf","orcid":"0000-0002-9978-8779","position":0,"is_corresponding":true}],"reference_count":10,"raw_metadata":null,"created_at":"2026-07-18T21:06:31.136481Z","pmid":"32609874","pmcid":null,"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":[]}