Preprint Concept Paper Version 2 Preserved in Portico This version is not peer-reviewed

Proposed O-GalNAc/Gal Glycosylation Pathways in Blood Group O and Non-O Blood Group Phenotypes During Plasmodium falciparum Infections. A Hypothesis Regarding how ABO(H) Blood Group Phenotype Formation Drives 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 Glycosylation Pathways in Blood Group O and Non-O Blood Group Phenotypes During Plasmodium falciparum Infections. A Hypothesis Regarding how ABO(H) Blood Group Phenotype Formation Drives Evolution. Preprints 2020, 2020050321 (doi: 10.20944/preprints202005.0321.v2). Arend, P. Proposed O-GalNAc/Gal Glycosylation Pathways in Blood Group O and Non-O Blood Group Phenotypes During Plasmodium falciparum Infections. A Hypothesis Regarding how ABO(H) Blood Group Phenotype Formation Drives 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). Nevertheless, this parasite breaks the species barrier via hijacking the host's A-like/Tn formation through abundantly expressed serine residues and creating hybrid A-like/Tn structures, associated with the arising of the germline-encoded nonimmune polyreactive immunoglobulin M (IgM), exerting the highly anti-A/B/H-aggressive isoagglutinin avtivities. In the human, this nonimmune antibody molecule physiologically undergoes the ABO(H) blood group phenotype formation, occurring on the surfaces of red blood cells (RBC), epithelial and endothelia cells as well as on plasma proteins by identical glycosylation, performed by the ABO(H) allelic, specific glycotransferases in a single enzymatic step, reducing and/or removing anti-A/B/H-reactive IgM, or isoagglutinin activities. ABO(H) phenotype diversity, this way glycosidically linked 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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