A large cohort study of the effects of Lewis, ABO, 13 other blood groups, and secretor status on COVID‐19 susceptibility, severity, and long COVID‐19

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Abstract

Background

Previous studies have reported Blood type O to confer a lower risk of SARS‐CoV‐2 infection, while secretor status and other blood groups have been suspected to have a similar effect as well.

Study design and methods

To determine whether any other blood groups influence testing positive for SARS‐CoV‐2, COVID‐19 severity, or prolonged COVID‐19, we used a large cohort of 650,156 Danish blood donors with varying available data for secretor status and blood groups ABO, Rh, Colton, Duffy, Diego, Dombrock, Kell, Kidd, Knops, Lewis, Lutheran, MNS, P1PK, Vel, and Yt.

Of these, 36,068 tested positive for SARS‐CoV‐2 whereas 614,088 tested negative between 2020‐02‐17 and 2021‐08‐04. Associations between infection and blood groups were assessed using logistic regression models with sex and age as covariates.

Results

The Lewis blood group antigen Le ^a displayed strongly reduced SARS‐CoV‐2 susceptibility OR 0.85 CI[0.79–0.93] p < .001. Compared to blood type O, the blood types B, A, and AB were found more susceptible toward infection with ORs 1.1 CI[1.06–1.14] p < .001, 1.17 CI[1.14–1.2] p < .001, and 1.2 CI[1.14–1.26] p < .001, respectively. No susceptibility associations were found for the other 13 blood groups investigated. There was no association between any blood groups and COVID‐19 hospitalization or long COVID‐19. No secretor status associations were found.

Discussion

This study uncovers a new association to reduced SARS‐CoV‐2 susceptibility for Lewis type Le ^a and confirms the previous link to blood group O. The new association to Le ^a could be explained by a link between mucosal microbiome and SARS‐CoV‐2.

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Most cited references 41

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A new method of classifying prognostic comorbidity in longitudinal studies: Development and validation

Mary Charlson, Peter Pompei, Kathy Ales … (1987)

The objective of this study was to develop a prospectively applicable method for classifying comorbid conditions which might alter the risk of mortality for use in longitudinal studies. A weighted index that takes into account the number and the seriousness of comorbid disease was developed in a cohort of 559 medical patients. The 1-yr mortality rates for the different scores were: "0", 12% (181); "1-2", 26% (225); "3-4", 52% (71); and "greater than or equal to 5", 85% (82). The index was tested for its ability to predict risk of death from comorbid disease in the second cohort of 685 patients during a 10-yr follow-up. The percent of patients who died of comorbid disease for the different scores were: "0", 8% (588); "1", 25% (54); "2", 48% (25); "greater than or equal to 3", 59% (18). With each increased level of the comorbidity index, there were stepwise increases in the cumulative mortality attributable to comorbid disease (log rank chi 2 = 165; p less than 0.0001). In this longer follow-up, age was also a predictor of mortality (p less than 0.001). The new index performed similarly to a previous system devised by Kaplan and Feinstein. The method of classifying comorbidity provides a simple, readily applicable and valid method of estimating risk of death from comorbid disease for use in longitudinal studies. Further work in larger populations is still required to refine the approach because the number of patients with any given condition in this study was relatively small.

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Genomewide Association Study of Severe Covid-19 with Respiratory Failure

David Ellinghaus, Frauke Degenhardt, Luis Bujanda … (2020)

Abstract Background There is considerable variation in disease behavior among patients infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus that causes coronavirus disease 2019 (Covid-19). Genomewide association analysis may allow for the identification of potential genetic factors involved in the development of Covid-19. Methods We conducted a genomewide association study involving 1980 patients with Covid-19 and severe disease (defined as respiratory failure) at seven hospitals in the Italian and Spanish epicenters of the SARS-CoV-2 pandemic in Europe. After quality control and the exclusion of population outliers, 835 patients and 1255 control participants from Italy and 775 patients and 950 control participants from Spain were included in the final analysis. In total, we analyzed 8,582,968 single-nucleotide polymorphisms and conducted a meta-analysis of the two case–control panels. Results We detected cross-replicating associations with rs11385942 at locus 3p21.31 and with rs657152 at locus 9q34.2, which were significant at the genomewide level (P<5×10−8) in the meta-analysis of the two case–control panels (odds ratio, 1.77; 95% confidence interval [CI], 1.48 to 2.11; P=1.15×10−10; and odds ratio, 1.32; 95% CI, 1.20 to 1.47; P=4.95×10−8, respectively). At locus 3p21.31, the association signal spanned the genes SLC6A20, LZTFL1, CCR9, FYCO1, CXCR6 and XCR1. The association signal at locus 9q34.2 coincided with the ABO blood group locus; in this cohort, a blood-group–specific analysis showed a higher risk in blood group A than in other blood groups (odds ratio, 1.45; 95% CI, 1.20 to 1.75; P=1.48×10−4) and a protective effect in blood group O as compared with other blood groups (odds ratio, 0.65; 95% CI, 0.53 to 0.79; P=1.06×10−5). Conclusions We identified a 3p21.31 gene cluster as a genetic susceptibility locus in patients with Covid-19 with respiratory failure and confirmed a potential involvement of the ABO blood-group system. (Funded by Stein Erik Hagen and others.)

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Microbiota Modulation of the Gut-Lung Axis in COVID-19

Gislane Lelis Vilela de Oliveira, Camilla Oliveira, Camila Figueiredo Pinzan … (2021)

COVID-19 is an infectious disease caused by the Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), and according to the World Health Organization (WHO), to date, SARS-CoV-2 has already infected more than 91.8 million people worldwide with 1,986,871 deaths. This virus affects mainly the respiratory system, but the gastrointestinal tract (GIT) is also a target, meanwhile SARS-CoV-2 was already detected in oesophagus, stomach, duodenum, rectum, and in fecal samples from COVID-19 patients. Prolonged GIT manifestations in COVID-19, mainly the diarrhea, were correlated with decreased richness and diversity of the gut microbiota, immune deregulation and delayed SARS-CoV-2 clearance. So, the bidirectional interactions between the respiratory mucosa and the gut microbiota, known as gut-lung axis, are supposed to be involved in the healthy or pathologic immune responses to SARS-CoV-2. In accordance, the intestinal dysbiosis is associated with increased mortality in other respiratory infections, due to an exacerbated inflammation and decreased regulatory or anti-inflammatory mechanisms in the lungs and in the gut, pointing to this important relationship between both mucosal compartments. Therefore, since the mucous membranes from the respiratory and gastrointestinal tracts are affected, in addition to dysbiosis and inflammation, it is plausible to assume that adjunctive therapies based on the modulation of the gut microbiota and re-establishment of eubiosis conditions could be an important therapeutic approach for constraining the harmful consequences of COVID-19. Then, in this review, we summarized studies showing the persistence of SARS-CoV-2 in the gastrointestinal system and the related digestive COVID-19 manifestations, in addition to the literature demonstrating nasopharyngeal, pulmonary and intestinal dysbiosis in COVID-19 patients. Lastly, we showed the potential beneficial role of probiotic administration in other respiratory infections, and discuss the possible role of probiotics as an adjunctive therapy in SARS-CoV-2 infection.

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Author and article information

Contributors

Camous Moslemi:

ORCID: https://orcid.org/0000-0001-7905-9774

camos@regionsjaelland.dk

Journal

Journal ID (nlm-ta): Transfusion

Journal ID (iso-abbrev): Transfusion

Journal ID (doi): 10.1111/(ISSN)1537-2995

Journal ID (publisher-id): TRF

Title: Transfusion

Publisher: John Wiley & Sons, Inc. (Hoboken, USA )

ISSN (Print): 0041-1132

ISSN (Electronic): 1537-2995

Publication date (Electronic): 03 November 2022

Publication date (Print): January 2023

Publication date PMC-release: 03 November 2022

Volume: 63

Issue: 1 ( doiID: 10.1111/trf.v63.1 )

Pages: 47-58

Affiliations

[ ¹ ] Department of Clinical Immunology Zealand University Hospital Køge Denmark

[ ² ] Department of Clinical Immunology Copenhagen University Hospital, Rigshopitalet Copenhagen Denmark

[ ³ ] Department of Clinical Immunology Aarhus University Hospital Skejby Denmark

[ ⁴ ] Novo Nordisk Foundation Center for Protein Research University of Copenhagen Copenhagen Denmark

[ ⁵ ] Department of Clinical Immunology Aalborg University Hospital Aalborg Denmark

[ ⁶ ] Department of Clinical Immunology Odense University Hospital Odense Denmark

[ ⁷ ] Danish Cancer Society Research Center Copenhagen Denmark

[ ⁸ ] Danish Big Data Centre for Environment and Health (BERTHA) Aarhus University Roskilde Denmark

[ ⁹ ] Department of Neurology NeuroGenomic group, Rigshospitalet Glostrup Denmark

[ ¹⁰ ] Statens Serum Institut Copenhagen Denmark

[ ¹¹ ] Department of Laboratory Medicine Lund University Lund Sweden

[ ¹² ] Department of Clinical Immunology and Transfusion Medicine Office for Medical Services Lund Sweden

[ ¹³ ] Department of Clinical Medicine, Faculty of Health and Medical Sciences University of Copenhagen Copenhagen Denmark

Author notes

[*] [* ] Correspondence

Camous Moslemi, Department of Clinical Immunology, Zealand University Hospital, Køge, Denmark.

Email: camos@ 123456regionsjaelland.dk

Author information

Camous Moslemi https://orcid.org/0000-0001-7905-9774

Thorsten Brodersen https://orcid.org/0000-0003-4431-9972

Maria Didriksen https://orcid.org/0000-0002-4856-496X

Joseph Dowsett https://orcid.org/0000-0001-5381-2633

Martin L. Olsson https://orcid.org/0000-0003-1647-9610

Article

Publisher ID: TRF17170

DOI: 10.1111/trf.17170

PMC ID: 9874484

PubMed ID: 36271437

SO-VID: 5afb805e-544f-472a-87f0-f4038aa59ee3

License:

This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

History

Date revision received : 15 August 2022

Date received : 11 February 2022

Date accepted : 14 September 2022

Page count

Figures: 0, Tables: 5, Pages: 12, Words: 7369

Custom metadata

source-schema-version-number 2.0

cover-date January 2023

details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_JATSPMC version:6.2.4 mode:remove_FC converted:26.01.2023

ScienceOpen disciplines: Hematology

Keywords: abo,blood antigen,blood groups,blood systems,covid hospitalization,covid severity,covid susceptibility,covid‐19,diego,dombrock,duffy,fut2,fut3,kell,kidd,knops,lewis,long covid symptoms,long covid‐19,lutheran,mns,p1pk,rh,sars‐cov‐2,secretor,vel,yt

Data availability:

ScienceOpen disciplines: Hematology

Keywords: abo, blood antigen, blood groups, blood systems, covid hospitalization, covid severity, covid susceptibility, covid‐19, diego, dombrock, duffy, fut2, fut3, kell, kidd, knops, lewis, long covid symptoms, long covid‐19, lutheran, mns, p1pk, rh, sars‐cov‐2, secretor, vel, yt

A large cohort study of the effects of Lewis, ABO, 13 other blood groups, and secretor status on COVID‐19 susceptibility, severity, and long COVID‐19

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Abstract

Background

Study design and methods

Results

Discussion

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Novel Coronavirus Disease COVID-19

Most cited references 41

A new method of classifying prognostic comorbidity in longitudinal studies: Development and validation

Genomewide Association Study of Severe Covid-19 with Respiratory Failure

Microbiota Modulation of the Gut-Lung Axis in COVID-19

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