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Approximately 45 percent of Caucasians are type O (positive or negative), but 51 percent of African-Americans and 57 percent of Hispanics are type O. Minority and diverse populations, therefore, play a critical role in meeting the constant need for blood.

Types O negative and O positive are in high demand. Only 7% of the population are O negative. However, the need for O negative blood is the highest because it is used most often during emergencies. The need for O+ is high because it is the most frequently occurring blood type (37% of the population).

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There are more than 600 other known antigens, the presence or absence of which creates "rare blood types." Your blood type is considered rare if you lack antigens that 99% of the people are positive for. If you somehow lack an antigen that 99.99% are positive for, your blood type is extremely rare.

* Note: If you have questions about paternity testing or about blood group inheritance, your primary care physician should be able to provide you with an appropriate referral. Testing difficulties can cause exceptions to the above patterns. ABO blood typing is not sufficient to prove or disprove paternity or maternity.

The Rh blood group system is one of the most polymorphic and immunogenic systems known in humans. In the past decade, intense investigation has yielded considerable knowledge of the molecular background of this system. The genes encoding 2 distinct Rh proteins that carry C or c together with either E or e antigens, and the D antigen, have been cloned, and the molecular bases of many of the antigens and of the phenotypes have been determined. A related protein, the Rh glycoprotein is essential for assembly of the Rh protein complex in the erythrocyte membrane and for expression of Rh antigens. The purpose of this review is to provide an overview of several aspects of the Rh blood group system, including the confusing terminology, progress in molecular understanding, and how this developing knowledge can be used in the clinical setting. Extensive documentation is provided to enable the interested reader to obtain further information. (Blood. 2000;95:375-387)

We report proportions for binary test results and occurrence of clinical outcomes with accompanying 95% exact confidence intervals (CIs). Equality of proportions between groups was tested using a likelihood ratio 2 test and evaluated at a 5% significance level. Because we had an a priori hypothesis about specific blood groups affecting the risk of infection, we computed RRs for contracting SARS-CoV-2 for each blood group. In a sensitivity analysis, we modeled the potential impact that overrepresentation of immigrants of nonwestern origin in the patient population could have on the estimated risk ratios. All analyses were done in Stata 16.

There was no difference (all P > .40) between ABO blood groups and clinical severity of COVID-19 for nonhospitalized patients vs hospitalized patients or for deceased patients vs living patients (Table 2).

Immigrants from nonwestern countries and their first-generation descendants are overrepresented among Danish COVID-19 patients (constituting 18% of cases but only 9% of the population),18 which could confound the ABO distribution among SARS-CoV-2+ individuals. Therefore, we performed a sensitivity analysis by calculating a weighted reference ABO distribution, taking into account the number of COVID-19 cases among immigrants from the nations constituting the largest sources of nonwestern immigration in Denmark (Pakistan, Morocco, Somalia, Turkey, and Iraq) and reference ABO distributions in their respective country of origin. Using this weighted ABO distribution as an alternative reference population, we reanalyzed and found an adjusted RR for blood group O individuals of 0.88 (supplemental Table 2), which was very similar to our initial result (RR, 0.87; Table 1).

Here, we demonstrate that blood group O is significantly associated with reduced susceptibility to SARS-CoV-2 infection. Additionally, ABO blood groups were not associated with rates of hospitalization or death following infection.

Our study has several limitations. ABO blood group information was only available for 62% of all tested individuals, and only doctors and nurses were identified as health care personnel. The sex of the tested population was skewed, with females accounting for 71% of those who screened negative and 67% of those who screened positive. However, blood groups are generally independent of sex. More importantly, however, is the fact that blood group distributions vary among ethnic subgroups with different susceptibility for infection. Indeed, a higher than expected contribution of immigrants from nonwestern countries is noted among Danish COVID-19 patients,18 but a sensitivity analysis indicated this is not a major bias and, thus, is unlikely to affect the overall conclusion.

The data presented here are consistent with other studies reporting primarily on hospitalized patients2-6 and those exploring SARS-CoV-1 susceptibility.7 Several hypotheses could explain these results. In vitro studies have indicated that SARS-CoV-1 particles can be glycosylated by the A variant of the ABO glycosyltransferases, allowing anti-A antibodies to neutralize the virus.11 Although not studied, it is likely to be the case for the B variant, as well, and, therefore, for anti-B antibodies. Because anti-A and anti-B are present on mucosal surfaces in some individuals lacking the corresponding ABO blood group,19 this might explain the relative protection of blood group O individuals. In this context, it is interesting that the highest RR for infection was found for blood group AB lacking both antibodies. However, the RR of group AB did not differ significantly from that of group A or B; because of the paucity of blood group AB, it would require a considerably larger number of patients to clarify this. Alternatively, the effect could be indirect, as a result of the association between ABO blood groups and levels of von Willebrand factor, which is higher in non-O individuals15 and who are also more prone to arterial and venous thrombosis,20 which are important comorbidities for COVID-19. Importantly, the majority of patients reported here were not hospitalized and, therefore, were less likely to have such comorbidities.

Our findings of similar relative protection by blood group O in young individuals, in health care personnel, and in individuals without a registered cardiovascular diagnosis suggest that associations between non-O blood groups and comorbidities do not explain the apparent protection enjoyed by group O individuals, in line with findings reported by Zietz and Tatonetti.3 Moreover, our data do not indicate an association between blood group and progression to hospitalization or death from COVID-19. This is consistent with data from Ellinghaus et al,6 who did not find any differences in the usage of oxygen or ventilation between ABO blood groups in hospitalized patients. Given the known increased risk of thrombosis in non-O individuals and the evolving central role for thrombosis in the pathogenesis of COVID-19, it is important to explore this aspect more closely in larger patient cohorts (eg, by examining ABO blood type and viral load, the severity of symptoms, and the long-term effects following COVID-19). Furthermore, it should be emphasized that the 2 hypotheses do not exclude each other.

A blood type (also known as a blood group) is a classification of blood, based on the presence and absence of antibodies and inherited antigenic substances on the surface of red blood cells (RBCs). These antigens may be proteins, carbohydrates, glycoproteins, or glycolipids, depending on the blood group system. Some of these antigens are also present on the surface of other types of cells of various tissues. Several of these red blood cell surface antigens can stem from one allele (or an alternative version of a gene) and collectively form a blood group system.[1]

A complete blood type would describe each of the 44 blood groups, and an individual's blood type is one of many possible combinations of blood-group antigens.[2] Almost always, an individual has the same blood group for life, but very rarely an individual's blood type changes through addition or suppression of an antigen in infection, malignancy, or autoimmune disease.[3][4][5][6] Another more common cause of blood type change is a bone marrow transplant. Bone-marrow transplants are performed for many leukemias and lymphomas, among other diseases. If a person receives bone marrow from someone of a different ABO type (e.g., a type O patient receives a type A bone marrow), the patient's blood type should eventually become the donor's type, as the patient's hematopoietic stem cells (HSCs) are destroyed, either by ablation of the bone marrow or by the donor's T-cells. Once all the patient's original red blood cells have died, they will have been fully replaced by new cells derived from the donor HSCs. Provided the donor had a different ABO type, the new cells' surface antigens will be different from those on the surface of the patient's original red blood cells.[citation needed]

Some blood types are associated with inheritance of other diseases; for example, the Kell antigen is sometimes associated with McLeod syndrome.[7] Certain blood types may affect susceptibility to infections, an example being the resistance to specific malaria species seen in individuals lacking the Duffy antigen.[8] The Duffy antigen, presumably as a result of natural selection, is less common in population groups from areas having a high incidence of malaria.[9]

The ABO blood group system involves two antigens and two antibodies found in human blood. The two antigens are antigen A and antigen B. The two antibodies are antibody A and antibody B. The antigens are present on the red blood cells and the antibodies in the serum. Regarding the antigen property of the blood all human beings can be classified into four groups, those with antigen A (group A), those with antigen B (group B), those with both antigen A and B (group AB) and those with neither antigen (group O). The antibodies present together with the antigens are found as follows:[citation needed] 2351a5e196