When according to the numbers of Wikipedia (although they are disputed) in countries like Chile, Ecuador, Colombia, Simbabwe and Mexico 59 to 85 percent of the people have blood group O and these countries officially publish extremely low COVID-19 cases and death rates per 1 million inhabitants, this may not alone result from insufficient investigations but might suggest a lower susceptibility of blood group O to the disease. The molecular biology of a virus infection pathogenesis determines

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... genetic target and the human phenotype-determining enzymes decide about the difference between infection and disease. In the case that O-glycosylation plays a key role in the pathogenesis of coronavirus infections, as was discussed already 14 years ago in a SARS-CoV virus infection and is currently again predicted for SARS-CoV-2 or COVID-19, this would involve the formation of hybrid, serologically A-like, O-GalNAcα1-Ser/Thr-R, Tn ("T nouvelle") antigenic structures. Although the ACE2 (angiotensin-converting-enzyme 2) protein is defined as the primary SARS-CoV receptor, it is the history of the amino acid serine, suggesting the actual or additional binding via an intermediate hybrid O-glycan. The protease-mobilized, virus-encoded serine molecule gets access to the host's N-acetyl-D-galactosamine (GalNAc) metabolism and the resulting intermediate, hybrid A-like/Tn structure performs the adhesion of the virus to host cells primarily independent of the ABO blood group, while the phenotype-determining sugars become the final glycosidic target: individuals with blood group A cannot respond with either acquired or innate antibodies to the synthesis of A-like hybrid structures due to clonal selection and phenotypic accommodation of plasma proteins but perform a further (blood group-A-specific) hybrid binding. A first statistical study suggests that people with blood group A have a significantly higher risk for acquiring COVID-19, whereas people with blood group O have a significantly lower risk for the infec [...]