How blood group A repairs the lack of the parasite Plasmodium falciparum’s synthesis of the aminosugar N-acetyl-D-galactosamine (GalNAc).
Upon infection, the abundantly expressed serine molecule of the parasite Plasmodium falciparum gains access to the GalNAc pathways of the host1 and produces an intermittent trans-species, hybrid Tn/ A-like antigen (Galα-1-O-Ser/Thr-R), catalysed by the developmental polypeptide GalNAc transferase and completed by blood group A-specific (A-allelic) glycosylation, resulting in the neutralisation of the anti-A/Tn reactivity of the pre-existing poly-reactive germline encoded immunoglobulin M (IgM). References: 1. Arend, P. Position of human blood group O(H) and phenotype-determining enzymes in growth and infectious disease. Annals of the New York Academy of Sciences vol. 1425 5–18 (2018).
