PreprintConcept PaperVersion 2Preserved in Portico This version is not peer-reviewed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.org2020, 2020050321. https://doi.org/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.org 2020, 2020050321. https://doi.org/10.20944/preprints202005.0321.v2
Cite as:
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.org2020, 2020050321. https://doi.org/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.org 2020, 2020050321. https://doi.org/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.
Biology and Life Sciences, Biochemistry and Molecular Biology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Commenter: Peter Arend
Commenter's Conflict of Interests: Author