Your blood type may affect y;our propensity for COVID-19 infection.
ABSTRACT
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 result in the formation of a serologically A-like, O-GalNAcα1-Ser/Thr-R, Tn (“T nouvelle”) antigenic structure. The adhesion of the virus to host cells would primarily occur independent of the ABO blood group through this intermediate, evolutionary/ developmental structure, which is common to all metazoan growth processes and apparently acts as a host-pathogen functional bridge in different, unrelated infectious diseases. 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, and would thus become a preferred target for the virus through a potentially blood group-specific (A-allelic) additional binding. In fact, apart from countless corresponding observations and presumptions, 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 observations might raise new questions on the immuno- and pharmaco- therapeutic target, blood group O people maintain the anti-A/Tn cross-reactive, complement-dependent isoagglutinin activity, which is exerted by the polyreactive, nonimmune immunoglobulin M (IgM), representing the humoral spearhead of innate immunity and a first line of defense.
Reference:
Arend, Peter (2020): How blood group A might be a risk and blood group O be protected from coronavirus (COVID-19) infections. figshare.
Preprint at https://doi.org/10.6084/m9.figshare.12019035.v45