Fig. 1.

The viral SARS-CoV-2 serine residues, mobilized by host’s TMPRSS2, highjack the host’s GalNAc metabolism and both blood group O(H) and blood group A are identically infected via blood group independent, trans-species intermediate A-like/Tn, O-GalNAcα1-Ser/Thr-R glycosylation. In blood group O(H) this intermediate hybrid structure is replaced by mucin-type fucosylation or H-antigen formation, which neutralizes the activity of innate anti-H isoagglutinin but leaves unaffected the activities of innate anti-A/Tn and anti-B isoagglutinins, exerted by the nonimmune polyreactive IgM, implicating a secondary IgG response. In blood group A, the intermediate Tn binding is hypothetically replaced by hybrid A-allelic mucin-type formation via mucin-type fucosylation. This involves the phenotypic accommodation of the polyreactive nonimmune IgM, downregulation of anti-A/Tn IgM (isoagglutinin) activities and decrease in the level of the anti-B IgM (isoagglutinin) activity, while anti-A/B reactive IgG formations are precluded by clonal selection. This figure was constructed according to ‘Fig. 2′ in a previous article (Arend, 2018a), in which this mechanism may be similarly utilized by a non-viral pathogen, such as the protozoan parasite Plasmodium falciparum.