Among the many aspects that characterize the COVID-19 pandemic, two seem particularly challenging to understand: i), the great geographical differences in the degree of virus contagiousness and lethality which were found in the different phases of the epidemic progression, and , ii) , the potential role of the infected people's blood type in both the virus infectivity and the progression of the disease. Recently, Breiman et al. (2020) presented a hypothesis that could shed some light on i) and ii), specifically, it has been proposed that during the subject-to-subject transfer SARS-CoV-2 conserves on its capsid the erythrocytes' antigens of the source subject , causing a potential immune reaction in a receiving subject which has previously acquired specific antibodies to the source subject antigens. This  implies a blood type-dependent infection rate. The strong geographical dependence of the blood type distribution could be, therefore, one of the factors at the origin of i). Here we present an epidemiological deterministic model where the infection rules hypothesized in Breiman et al. (2020) are taken into account . The comparison of the model outcome with exiting worldwide infection progression data seems to support the Breiman et al. (2020) hypothesis .
Among the many aspects that characterize the COVID-19 pandemic, two seem particularly challenging to understand: (i) the great geographical differences in the degree of virus contagiousness and lethality which were found in the different phases of the epidemic progression, and (ii) the potential role of the infected people's blood type in both the virus infectivity and the progression of the disease. A recent hypothesis could shed some light on both aspects. Specifically, it has been proposed that in the subject-to-subject transfer SARS-CoV-2 conserves on its capsid the erythrocytes' antigens of the source subject . Thus these conserved antigens can potentially cause an immune reaction in a receiving subject that has previously acquired specific antibodies for the source subject antigens. This hypothesis implies a blood type-dependent infection rate. The strong geographical dependence of the blood type distribution could be, therefore, one of the factors at the origin of the observed heterogeneity in the epidemics spread. Here, we present an epidemiological deterministic model where the infection rules based on blood types are taken into account and compare our model outcomes with the exiting worldwide infection progression data . We found an overall good agreement, which strengthens the hypothesis that blood types do play a role in the COVID-19 infection .
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