While the attachment of the virus to the host occurs independent of the ABO blood group, patients with blood group “A” cannot respond with either innate or acquired antibodies to the synthesis of the hybrid “A” structure due to clonal selection and phenotypic, glycosidic accommodation of plasma proteins. The virus cannot survive outside of its hosts and hypothetically utilizes the hosts machinery by attaching to A-like (O-GalNAcα1-Ser/Thr-R, Tn) antigenic structure via serine rich motifs. Īnother proposed mechanism described by Oostra et al reported that O-glycosylation plays a key role in the pathogenesis of coronavirus infection. This is supported by the study of Zhao et al, in which patients with type A blood had higher risk of COVID-19 infection. As suggested in prior study of SARS-CoV-2 infections, the adhesion of spike protein to the ACE2 receptor on the host cell surface may be inhibited by the presence of anti-A antibody, thereby conferring protection to those with non-type A blood. While no concrete mechanism for association between blood groups and infection risk for COVID-19 has been identified, two different mechanisms of how ABO blood type could play a role have been proposed.Įntry of SARS-CoV-2 into human cells has been shown to occur via the angiotensin-converting enzyme 2 (ACE2) receptor via the coronavirus spike protein and the association of disease susceptibility and receptor expression has been hypothesized. The association between ABO blood type and risk of infection has been described in two recent publications from China. As the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has spread rapidly around the world, limited evidence has identified the possibility that certain populations are at an increased risk of acquiring the infection and mortality. The novel coronavirus disease 2019 (COVID-19) was declared a pandemic by the World Health Organization (WHO) on Ma.
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