Your blood type is determined by genes you inherit from your biological parents. Specifically, a single gene on chromosome 9 controls whether your red blood cells display A antigens, B antigens, both, or neither. A second gene on chromosome 1 determines your Rh status (positive or negative). Together, these two genes produce the eight common blood types: A+, A−, B+, B−, AB+, AB−, O+, and O−.
The ABO Gene and Its Three Alleles
The ABO gene comes in three versions, called alleles: A, B, and O. You inherit one allele from each parent, giving you two copies total. The combination you receive dictates your blood type.
The A and B alleles each code for an enzyme that attaches a specific sugar molecule to the surface of your red blood cells. The A enzyme attaches a sugar called N-acetylgalactosamine, creating the A antigen. The B enzyme attaches a different sugar, galactose, creating the B antigen. These two enzymes are remarkably similar proteins, both 354 amino acids long, differing at only four positions. Those four tiny differences are enough to change which sugar each enzyme grabs and sticks onto the cell.
The O allele is essentially a broken version of the gene. Most O alleles have a single deleted DNA letter (a missing guanine at position 261) that throws off the reading frame, producing a nonfunctional enzyme. Without a working enzyme, no extra sugar gets added. The red blood cell is left with just the base structure, called the H antigen, sitting on its surface.
How Inheritance Creates Eight Blood Types
Because you carry two copies of the ABO gene, your blood type depends on which combination you received. A and B are both dominant over O, meaning you only need one working copy to produce that antigen. A and B are codominant with each other, so if you inherit one of each, both antigens appear on your cells. Here’s how the combinations play out:
- Two A alleles (AA) or one A and one O (AO): Type A
- Two B alleles (BB) or one B and one O (BO): Type B
- One A and one B allele (AB): Type AB
- Two O alleles (OO): Type O
This is why two parents with type A blood can have a child with type O. If both parents carry the hidden O allele (genotype AO), there’s a 25% chance their child inherits O from both sides and ends up OO. There’s a 50% chance the child is AO (type A) and a 25% chance they’re AA (also type A), giving the child a 75% overall probability of being type A and a 25% chance of being type O.
The Rh Factor: Positive or Negative
The second piece of your blood type is the Rh factor, a protein on the surface of red blood cells controlled by the RHD gene on chromosome 1. If you have at least one functional copy of this gene, you produce the Rh protein and are Rh-positive. If both copies are nonfunctional or deleted, you’re Rh-negative.
Rh-positive is dominant, so a person who is Rh-positive may carry one silent Rh-negative allele. Two Rh-positive parents can have an Rh-negative child if both carry that recessive allele. Two Rh-negative parents will always have Rh-negative children. About 77% of people are Rh-positive.
How Common Each Blood Type Is
Blood type distribution varies by population, but data from a large donor pool gives a useful snapshot. O-positive is the most common type at about 36%, followed by A-positive at 28%. B-positive accounts for roughly 8%, and AB-positive is the rarest common type at around 2%. Among Rh-negative types, O-negative makes up about 14%, A-negative 8%, B-negative 3%, and AB-negative just 1%.
These percentages shift significantly across ethnic and geographic populations, which reflects thousands of years of evolutionary pressure and population movement.
Why Blood Type Matters for Transfusions
Your immune system produces antibodies against whichever ABO antigens your own red blood cells lack. If you’re type A, your plasma contains anti-B antibodies. Type B individuals carry anti-A antibodies. Type O individuals carry both anti-A and anti-B. Type AB individuals carry neither.
This is why mismatched transfusions are dangerous. If type A blood enters someone with type B, their anti-A antibodies attack the donated red blood cells, potentially triggering a severe immune reaction. The same principle applies to Rh factor: an Rh-negative person can develop antibodies against Rh-positive blood after exposure, which is particularly important during pregnancy if a mother is Rh-negative and her baby is Rh-positive.
The Hidden Layer: The H Antigen
There’s a step before A and B that most people never think about. Before the A or B enzyme can do its job, a different gene called FUT1 (on chromosome 19) must first build the H antigen, which serves as the foundation. The A and B enzymes then modify this H antigen by adding their respective sugars on top of it.
In extremely rare cases, a person inherits two broken copies of FUT1. Without the H antigen foundation, neither A nor B antigens can be built, regardless of what ABO alleles the person carries. This is called the Bombay phenotype, and it’s one of the rarest blood types in the world. Someone with the Bombay phenotype may carry perfectly functional A or B genes but can’t express them. Their blood tests as type O, yet it’s incompatible with regular type O blood because they also produce antibodies against the H antigen itself. They can safely receive blood only from other individuals with the Bombay phenotype.
Why These Blood Types Exist at All
The persistence of different blood types across human populations isn’t random. Infectious diseases, particularly malaria, have exerted powerful evolutionary pressure on red blood cell characteristics for millennia. The geographic distribution of certain blood cell variants closely mirrors regions where malaria has historically been most intense.
Type O blood offers a striking example. People with type O have a 66% lower risk of severe malaria compared to those with types A, B, or AB. The mechanism is surprisingly direct: the malaria parasite Plasmodium falciparum uses a protein to create “rosettes,” clumps of infected and uninfected red blood cells that help the parasite evade the immune system and block small blood vessels. The A and B sugars on red blood cells strengthen these rosette bonds. O-type cells, which lack those sugars, reduce rosette formation by 60 to 70%, making it much harder for the parasite to cause severe disease.
Malaria has shaped other blood cell surface features too. In West and Central Africa, over 95% of people lack the Duffy blood group antigen, which one species of malaria parasite uses as a doorway to enter red blood cells. Without that receptor, the parasite simply can’t get in. In coastal Papua New Guinea, where malaria is extremely common, nearly half the population carries a variant of another blood group (Gerbich-negative) that cuts parasite invasion efficiency by 40 to 60%. In parts of East Africa, a variant called Dantu provides such strong protection that in one controlled infection study, none of the 30 carriers reached the threshold for treatment, compared to about 23% of non-carriers.
These patterns reveal blood type not as a fixed curiosity on a lab report but as a living record of how human populations adapted to the diseases that surrounded them over thousands of generations.