Blood Type Calculator

Blood type inheritance follows Mendel's first law (Law of Segregation, 1865) and is determined by two independent loci: the ABO gene on chromosome 9q34.2, which has three major alleles IA, IB, and IO (the i and superscripts are the modern notation, replacing the older A, B, O), and the RHD gene on chromosome 1p36.11, which has the D-positive dominant allele and the d-negative recessive allele. The IA and IB alleles encode distinct glycosyltransferases that modify the H antigen on the red blood cell surface into A or B antigens, while the IO allele is a deletion mutant (a single base deletion at position 261 in exon 6 that introduces a frameshift) producing a non-functional enzyme, so the H antigen remains unmodified and the cell presents as blood type O. Each person inherits one allele from each parent, giving the six genotypes IAIA, IAIO, IBIB, IBIO, IAIB, and IOIO that map to the four phenotypes A, A, B, B, AB, and O. The Punnett square is the standard tool for visualising the cross. The calculator enumerates all 36 possible parental genotype combinations (6x6), then computes the offspring genotype distribution by combining one allele from each parent. Because the page only knows the parents' phenotypes, an A parent can be IAIA or IAIO with equal prior probability (50/50) under the standard assumption, and the calculator averages the two cases. For Rh, a positive parent is either DD or Dd, and the page applies the same Hardy-Weinberg-style averaging. The result is a probability table for the four ABO phenotypes and the two Rh outcomes, presented as percentages that sum to 100. The chi-square test (Pearson 1900) is the standard statistic for testing whether observed offspring ratios match a Mendelian model, which is what a real serology lab would use to confirm a parentage claim. The calculator does not cover the rare phenotypes that surface in real transfusion work: the cis-AB allele (a single gene producing both A and B transferase activities, common in Korean and Japanese populations at 0.05% frequency), the weak D phenotype (a D antigen with reduced surface density, requires the indirect antiglobulin test to detect), the Bombay hh phenotype (no H antigen at all, so A and B transferases have no substrate), and the para-Bombay variant. These are the cases where the model output disagrees with a real serology report, and the page labels them explicitly. The Rh-null phenotype is a 1-in-6-million rarity; the Duffy null Fy(a-b-) is common in West African populations and confers resistance to Plasmodium vivax malaria. Migration advice: if a production system uses blood type for any clinical decision, never replace a real antigen typing laboratory test with a Mendelian prediction; the inheritance logic is fine for education and family-curiosity use, but transfusion, pregnancy, and forensic parentage all need real serology and a chain-of-custody document.

• ABO gene on chromosome 9q34.2: three alleles IA, IB, IO; IA and IB are codominant, both dominant over IO; six genotypes (IAIA, IAIO, IBIB, IBIO, IAIB, IOIO) map to four phenotypes A, A, B, B, AB, O.
• RHD gene on chromosome 1p36.11: D positive dominant over d negative; heterozygous Dd expresses D antigen; the page treats DD and Dd equally when only phenotype is known.
• Mendelian Law of Segregation (Mendel 1865, rediscovered 1900 by de Vries, Correns, and von Tschermak): the page implements the standard Punnett square (Punnett 1905) by enumerating all 36 parental genotype combinations, then averaging across the unknown genotypes for each phenotype input.
• O allele biology: IO is a single base deletion at position 261 in exon 6 of the ABO gene, introducing a frameshift that produces a non-functional glycosyltransferase; this is why O lacks the A and B antigens and why IO is recessive to IA and IB.
• Phenotype probability with unknown genotype: an A parent is 50% IAIA and 50% IAIO under the standard equal-prior assumption, so the offspring table is the weighted average of the two cases; the page exposes the prior explicitly so users can change it for populations with documented allele frequency skew.
• Rare phenotypes not modelled: cis-AB (Korea/Japan 0.05%), weak D, Bombay hh, para-Bombay, Rh-null (1 in 6 million), Duffy Fy(a-b-) (West Africa); a real serology mismatch means the model is incomplete, not wrong; defer to formal antigen typing and clinical records for transfusion, pregnancy, and forensic work.
• Rh clinical note: hemolytic disease of the newborn (HDN) happens when an Rh-negative mother carries an Rh-positive fetus and produces anti-D antibodies; the calculator ignores this and the Rh immunoglobulin (Rho(D) immune globulin, licensed 1968) prophylaxis that prevents it, so any pregnancy-related Rh question needs a clinician, not a Mendelian model.