Evidence map›Paper›PMID 33706067›Full record

ReviewImmunobiology2021

Why blood group A individuals are at risk whereas blood group O individuals are protected from SARS-CoV-2 (COVID-19) infection: A hypothesis regarding how the virus invades the human body via ABO(H) blood group-determining carbohydrates.

Peter Arend

Open access · hybridAbstract readReview
In one paragraph

Review in Immunobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.0field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 34 citations in OpenAlex.

  1. Seroprevalence of West Nile virus among blood donors in mainland France, 2021 to 2022.Euro surveillance : bulletin Europeen sur les maladies transmissibles = European communicable disease bulletin · 2026
    Article
  2. Article
  3. Observational
  4. Vitamin D status and blood group among severe COVID-19 patients.Annals of medicine and surgery (2012) · 2023
    Article
  5. Blood-Type-A is a COVID-19 infection and hospitalization risk in a Turkish cohort.Transfusion clinique et biologique : journal de la Societe francaise de transfusion sanguine · 2023
    Article
  6. Association Between ABO Blood Group System and COVID-19 Severity.American journal of clinical pathology · 2022
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Host polymorphisms and COVID-19 infection.Advances in clinical chemistry · 2022
    Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Peter ArendPhilipps University Marburg, Department of Medicine, D-355 Marburg, Lahn, Germany(2); Gastroenterology Research Laboratory, University of Iowa, Carver College of Medicine, Iowa City, IA 52242, USA(2); Research Laboratories, Chemie Grünenthal GmbH, D-52062 Aachen, Germany(2). Electronic address: parend@t-online.de.
Philipps University of Marburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

While the angiotensin converting enzyme 2 (ACE2) protein is defined as the primary severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) receptor, the viral serine molecule might be mobilized by the host's transmembrane protease serine subtype 2 (TMPRSS2) enzyme from the viral spike (S) protein and hijack the host's N-acetyl-D-galactosamine (GalNAc) metabolism. The resulting hybrid, serologically A-like/Tn (T nouvelle) structure potentially acts as a host-pathogen functional molecular bridge. In humans, this intermediate structure will hypothetically be replaced by ABO(H) blood group-specific, mucin-type structures, in the case of infection hybrid epitopes, implicating the phenotypically glycosidic accommodation of plasma proteins. The virus may, by mimicking the synthetic pathways of the ABO(H) blood groups, bind to the cell surfaces of the blood group O(H) by formation of a hybrid H-type antigen as the potential precursor of hybrid non-O blood groups, which does not affect the highly anti-glycan aggressive anti-A and anti-B isoagglutinin activities, exerted by the germline-encoded nonimmune immunoglobulin M (IgM). In the non-O blood groups, which have developed from the H-type antigen, these IgM activities are downregulated by phenotypic glycosylation, while adaptive immunoglobulins might arise in response to the hybrid A and B blood group structures, bonds between autologous carbohydrates and foreign peptides, suggesting the exertion of autoreactivity. The non-O blood groups thus become a preferred target for the virus, whereas blood group O(H) individuals, lacking the A/B phenotype-determining enzymes and binding the virus alone by hybrid H-type antigen formation, have the least molecular contact with the virus and maintain the critical anti-A and anti-B isoagglutinin activities, exerted by the ancestral IgM, which is considered the humoral spearhead of innate immunity.

Indexed as

AnimalsBlood Group AntigensCarbohydrate MetabolismCOVID-19Disease ResistanceHumansImmunoglobulin MPhenotypeRiskSARS-CoV-2Blood Group AntigensImmunoglobulin MA-like/Tn structureCOVID-19SARS-CoV-2–human carbohydrate interactionTrans-species glycan bridgeTrans-species glycosylation

Identifiers

PMID33706067
PMCPMC7609233
OpenAlexW3022938102

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.