Genetic factors such as ABO blood type and ACE2 receptor can also account for the unnatural link between malaria and COVID-19 . Humans have been infected and co-evolved with malaria . Numerous human polymorphisms are associated with this process of natural selection . Genetic variants for malaria may also contribute to the incidence and severity of SARS-CoV-2 infections (for example, ACE2 receptors) . There are four glycoproteins in humans: A, B, C, and D. These glycoproteins contain sialylated O-glycans and/or N-glycans. They interact with the Plasmodium falciparum ligands EBA-175, EBL-1, EBA-140, and EBA-140, respectively . Gerbich antigens are expressed on glycophorin C (GPC) and glycophorin D (GPD) . Generally, Gerbich antibodies do not result in severe hemolytic transfusion reactions (HTR) . Autoantibodies directed against Ge2 or Ge3 can result in autoimmune hemolytic anemia (AIHA) . During the initial adhesion phase of malaria parasites invading red blood cells, the merozoite surface protein 1-glycophore protein A-band 3 (MSP1-GPA-band 3) complex exerts its influence . Plasmodium falciparum cannot infect red blood cells deficient in glycoproteins A and B (M k phenotype) . COVID-19 infection and mortality rates are skewed toward patients with blood type A and away from those with blood type O . Patients with type O have natural IgM antibodies against both anti-A and anti-B. These antibodies may contribute to the host's viral load reduction and result in milder symptoms . SARS-CoV-1 exhibits similar characteristics . Thus, malaria and COVID-19 blood type infection rules are identical. Similar hemolytic reactions will occur if SARS-COV-2 has the same structure to invade red blood cells.