Abstract
The SARS‐CoV‐2 virus causes COVID‐19, an infection capable of causing severe disease and death but which can also be asymptomatic or oligosymptomatic. We investigated whether ABO blood group or secretor status was associated with COVID‐19 severity. We investigated secretor status because expression of ABO glycans on secreted proteins and non‐erythroid cells are controlled by a fucosyltransferase (FUT2), and inactivating FUT2 mutations result in a non‐secretor phenotype which protects against some viral infections. Data combined from healthcare records and our own laboratory tests (n = 275) of hospitalized SARS‐CoV‐2 polymerase chain reaction positive patients confirmed higher than expected numbers of blood group A individuals compared to O (RR = 1.24, CI 95% [1.05, 1.47], p = 0.0111). There was also a significant association between group A and COVID‐19‐related cardiovascular complications (RR = 2.56, CI 95% [1.43, 4.55], p = 0.0011) which is independent of gender. Molecular analysis revealed that group A non‐secretors are significantly less likely to be hospitalized than secretors. Testing of convalescent plasma donors, among whom the majority displayed COVID‐19 symptoms and only a small minority required hospitalization, group A non‐secretors were slightly over‐represented. Our findings showed that group A non‐secretors are not resistant to infection by SARS‐CoV‐2, but are more likely to experience a less severe form of associated disease.
Highlights
Genetic diversity among members of animal species including Homo sapiens is essential for their survival in response to newly emergent and evolving pathogens [1]
ABH antigen secretor status was determined by allele-specific polymerase chain reaction (PCR) of the G428A polymorphism in the FUT2 gene
Multiple other studies carried out in other countries have supported an association between ABO type and SARS-CoV-2 susceptibility to infection and/or outcomes [24,25,26,27]
Summary
Genetic diversity among members of animal species including Homo sapiens is essential for their survival in response to newly emergent and evolving pathogens [1]. Human blood group antigens are among the first polymorphic structures encountered by viruses and bacteria upon airborne contact with respiratory, gastrointestinal and urinogenital mucosal surfaces [2]. In the presence of active FUT2 A, B, H, and Leb antigens can be expressed on mucosal surfaces. Individuals with this phenotype are known as secretors [5,6]. In individuals lacking active FUT2, known as non-secretors, only the Lea antigen can be expressed [5]. There are several well studied interactions between host cells and both bacteria (Helicobacter pylori, Vibrio cholera) and viruses (noroviruses, rotaviruses) which are known to depend on the presence of these antigens [7,8]. It is clearly established that common strains of norovirus and rotavirus fail to infect non-secretors [9,10,11,12]
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