How blood group A might be a risk and blood group O be protected from coronavirus (COVID-19) infections

Peter Arend
2020 Figshare  
In the case that O-glycosylation plays a key role in the pathogenesis of coronavirus infections, as was discussed already 14 years ago and is currently again predicted, this would involve the formation of hybrid, serologically A-like, O-GalNAcα1-Ser/Thr-R, Tn ("T nouvelle") antigenic structures; the virus hypothetically hijacks the metabolism of the host's amino sugar N-acetyl-D-galactosamine (GalNAc) by serine-rich peptides. The resulting intermediate, evolutionary/developmental A-like/Tn
more » ... ntal A-like/Tn structure, which is common to all metazoan growth processes and apparently acts as a host-pathogen functional bridge in different, unrelated infectious diseases, would perform the adhesion of the virus to host cells primarily independent of the ABO blood group. However, while susceptibility to an infection and its severity depend on many factors, individuals with blood group A could not respond with either acquired or innate antibodies to the synthesis of A-like hybrid structures due to clonal selection and phenotypic accommodation of plasma proteins; blood group A individuals would become a preferred target for the virus, which utilizes the ACE receptor-mediated, blood group A-phenotype-determining enzyme activity and performs a further (blood group-A-specific) hybrid binding. In fact, a first statistical study suggests that people with blood group A have a significantly higher risk for acquiring COVID-19, whereas people with blood group O have a significantly lower risk for the infection compared with non-O blood groups (Zhao, J. et al., 2020). While these findings await confirmations, Chile, where 85% of people have blood group O, appears to have the lowest COVID 19 cases and death rates per 1 million inhabitants. Blood group O individuals, lacking the blood group-A-determining enzyme, may develop the least molecular contact with the virus and maintain the anti-A/Tn cross-reactive, complement-dependent isoagglutinin activity, which is exerted by the polyreactive, nonimmune immunoglobulin M (IgM), represe [...]
doi:10.6084/m9.figshare.12019035.v62 fatcat:h5aropgb25du3jq4qtvrrtl3wi