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Association between ABO blood types and coronavirus disease 2019 (COVID-19), genetic associations, and underlying molecular mechanisms: a literature review of 23 studies

Authors
  • Zhang, Yujia1
  • Garner, Rachael1
  • Salehi, Sana1
  • La Rocca, Marianna1
  • Duncan, Dominique1
  • 1 University of Southern California,
Type
Published Article
Journal
Annals of Hematology
Publisher
Springer-Verlag
Publication Date
Mar 08, 2021
Pages
1–10
Identifiers
DOI: 10.1007/s00277-021-04489-w
PMID: 33686492
PMCID: PMC7939543
Source
PubMed Central
Keywords
License
Unknown

Abstract

An association of various blood types and the 2019 novel coronavirus disease (COVID-19) has been found in a number of publications. The aim of this literature review is to summarize key findings related to ABO blood types and COVID-19 infection rate, symptom presentation, and outcome. Summarized findings include associations between ABO blood type and higher infection susceptibility, intubation duration, and severe outcomes, including death. The literature suggests that blood type O may serve as a protective factor, as individuals with blood type O are found COVID-19 positive at far lower rates. This could suggest that blood type O individuals are less susceptible to infection, or that they are asymptomatic at higher rates and therefore do not seek out testing. We also discuss genetic associations and potential molecular mechanisms that drive the relationship between blood type and COVID-19. Studies have found a strong association between a locus on a specific gene cluster on chromosome three (chr3p21.31) and outcome severity, such as respiratory failure. Cellular models have suggested an explanation for blood type modulation of infection, evidencing that spike protein/Angiotensin-converting enzyme 2 (ACE2)-dependent adhesion to ACE2-expressing cell lines was specifically inhibited by monoclonal or natural human anti-A antibodies, so individuals with non-A blood types, specifically O, or B blood types, which produce anti-A antibodies, may be less susceptible to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection due to the inhibitory effects of anti-A antibodies.

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