Preprint Concept Paper Version 1 This version is not peer-reviewed

How Blood Group A Might Be a Risk and Blood Group O Be Protected from SARS-CoV-2 (COVID-19) Infections (How the Virus Invades the Human Body via ABO(H) Blood Group-Determining Carbohydrates)

Version 1 : Received: 5 May 2020 / Approved: 6 May 2020 / Online: 6 May 2020 (14:41:35 CEST)

How to cite: Arend, P. How Blood Group A Might Be a Risk and Blood Group O Be Protected from SARS-CoV-2 (COVID-19) Infections (How the Virus Invades the Human Body via ABO(H) Blood Group-Determining Carbohydrates). Preprints 2020, 2020050097 (doi: 10.20944/preprints202005.0097.v1). Arend, P. How Blood Group A Might Be a Risk and Blood Group O Be Protected from SARS-CoV-2 (COVID-19) Infections (How the Virus Invades the Human Body via ABO(H) Blood Group-Determining Carbohydrates). Preprints 2020, 2020050097 (doi: 10.20944/preprints202005.0097.v1).

Abstract

While the angiotensin-converting-enzyme 2 (ACE2) is defined as the primary SARS-CoV-2 receptor (Severe acute respiratory syndrome-related coronavirus), the virus-encoded serine molecule, mobilized by the host’s TMPRSS2 (transmembrane protease serine subtype 2) from the viral (S) spike protein, hijacks the N-acetyl-D-galactosamine (GalNAc) metabolism of the host, and the resulting hybrid, serologically A-like/Tn (T-nouvelle) structure may perform the adhesion of the virus to host cells. In humans, this intermediate structure will hypothetically be replaced by ABO(H) blood group-specific, mucin-type, in the case of infection hybrid epitopes, implicating the phenotypically glycosidic accommodation of plasma proteins. The virus may, mimicking the synthetic pathways of the ABO(H) blood groups, bind to the cell surfaces of the blood group O(H) by formation of a hybrid H-type antigen or hybrid precursor of the non-O blood groups, which does not affect the highly anti-glycan aggressive anti-A and anti-B isoagglutinin activities, exerted by the germline-encoded nonimmune immunoglobulin M (IgM). In the non-O blood groups, which have developed from the H-type-antigen, these activities are downregulated by phenotypic glycosylation, while adaptive immunoglobulins might arise in response against the hybrid A and B blood group structures, which suggesting to exert autoreactivity. The non-O blood groups thus become a preferred target for the virus, whereas blood group O(H) individuals, lacking the A/B phenotype-determining enzymes and binding the virus alone by hybrid H-type antigen formation, have the least molecular contact to the virus and maintain the critical anti-A and anti-B isoagglutinin activities, exerted by the ancestral IgM, which is considered the humoral spearhead of innate immunity.

Supplementary and Associated Material

Subject Areas

COVID-19; SARS-CoV-2- human carbohydrate interaction; trans-species glycosylation; A-like/Tn formation; glycan trans-species bridge

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