Preprint Concept Paper Version 2 Preserved in Portico This version is not peer-reviewed

Proposed O-GalNAc/Gal Gycosylation Pathways in Blood Group O and Non-O Blood Group Phenotypes During Plasmodium falciparum Infections Driving Evolution

Version 1 : Received: 19 May 2020 / Approved: 20 May 2020 / Online: 20 May 2020 (07:03:37 CEST)
Version 2 : Received: 11 January 2021 / Approved: 12 January 2021 / Online: 12 January 2021 (12:33:29 CET)

How to cite: Arend, P. Proposed O-GalNAc/Gal Gycosylation Pathways in Blood Group O and Non-O Blood Group Phenotypes During Plasmodium falciparum Infections Driving Evolution. Preprints 2020, 2020050321 (doi: 10.20944/preprints202005.0321.v2). Arend, P. Proposed O-GalNAc/Gal Gycosylation Pathways in Blood Group O and Non-O Blood Group Phenotypes During Plasmodium falciparum Infections Driving Evolution. Preprints 2020, 2020050321 (doi: 10.20944/preprints202005.0321.v2).

Abstract

The coevolution of species drives diversity in animals and plants and contributes to natural selection, whereas in host–parasite coevolution, a parasite may complete an incomplete evolutionary/developmental function by utilizing the host cell’s machinery. Analysis of related older data suggests that Plasmodium falciparum (P. falciparum), the pathogen of malaria tropica, cannot survive outside its human host because it is unable to perform the evolutionarily first protein glycosylation of serologically A-like, O-GalNAcα1-Ser/Thr-R, Tn antigen (“T nouvelle”) formation, owing to its inability for synthesizing the amino sugar N-acetyl-d-galactosamine (GalNAc). This parasite breaks the species barrier via hijacking the host's physiological A-like/Tn formation through abundantly expressing serine residues and creating hybrid A-like/Tn structures, which in the human blood group O(H) are attacked by the germline-encoded nonimmune polyreactive immunoglobulin M (IgM), exerting the highly anti-A/B/H-aggressive isoagglutinin activities. These activities physiologically undergo the ABO(H) blood group phenotype formation, occurring on the surfaces of red blood cells (RBC), epithelial and endothelial cells and on plasma proteins by identical glycosylation, performed by the ABO(H)-allelic glycotransferases, phenotypically downregulating the anti-A/B/H-reactive IgM (isoagglutinin) activities in the non-O blood groups. ABO(H) phenotype diversity, this way glycosidically linked and molecularly connected to humoral immunity, becomes exposed to the evolution.

Supplementary and Associated Material

Subject Areas

trans-species O-glycosylation; trans-species functional bridge; phenotype-specific plasma glycosylation; glycosidic exclusion; ontogenetic Tn formation

Comments (1)

Comment 1
Received: 12 January 2021
Commenter: Peter Arend
Commenter's Conflict of Interests: Author
Comment: new title, new abstract, corrected figure 4
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