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A-

A- blood type, also known as A negative, is a human blood group within the ABO and Rh classification systems, defined by the presence of A antigens on the surface of red blood cells and the absence of the Rh (D) antigen.^[1] Individuals with A- blood naturally produce anti-B antibodies in their plasma, which can react against B antigens if incompatible blood is transfused.^[2] This blood type constitutes approximately 6% of the population in the United States and Canada, making it relatively uncommon compared to more prevalent types like O+ or A+.^[3]^[4] In terms of transfusion compatibility, A- blood is versatile as a donor: red blood cells from A- donors can be safely given to recipients with A+, A-, AB+, or AB- blood types, while A- plasma is compatible with A and AB recipients.^[5] Conversely, individuals with A- blood can only receive red blood cells from A- or O- donors to avoid hemolytic reactions caused by Rh incompatibility.^[1] This specificity underscores the importance of blood typing in medical procedures such as surgeries, trauma care, and organ transplants, where mismatched transfusions can lead to severe immune responses.^[6] The inheritance of A- blood type follows Mendelian genetics, with the A allele being codominant over O but the Rh-negative trait being recessive, requiring both parents to contribute the relevant genes for a child to express A-.^[7]

Overview

Definition and Antigens

The A- blood type is defined by the presence of A antigens on the surface of red blood cells (RBCs) and the absence of B antigens, in combination with the absence of the Rh(D) antigen.^[2]^[8] This phenotype arises within the ABO blood group system, which classifies blood based on carbohydrate antigens A and/or B, and the Rh blood group system, which primarily assesses the presence or absence of the Rh(D) protein antigen on RBCs.^[2]^[8] In the plasma of A- individuals, anti-B antibodies (primarily IgM and IgG) are naturally occurring and target B antigens on incompatible RBCs, potentially leading to agglutination or hemolysis.^[2] Anti-Rh(D) antibodies, however, are not naturally present in Rh(D)-negative plasma but develop as IgG alloantibodies following immunization by exposure to Rh(D)-positive blood, such as via transfusion or fetomaternal hemorrhage.^[8] The A antigens are oligosaccharide chains attached to proteins or lipids on the RBC membrane, forming glycoproteins or glycolipids that extend outward from the cell surface; these chains terminate in an N-acetylgalactosamine residue as the immunodominant sugar.^[2] This structure is synthesized by a specific glycosyltransferase enzyme encoded by the ABO gene.^[2] A- blood differs from A+ blood, which expresses the same A antigens but also bears the Rh(D) antigen, and from O- blood, which lacks both A and B antigens while sharing the Rh(D)-negative status.^[1]^[5]

Global Prevalence

The A- blood type accounts for approximately 3% of the global population, making it one of the rarer combinations within the ABO and Rh systems.^[9] This estimate derives from aggregated data on blood group distributions, reflecting the overall scarcity of the Rh-negative factor worldwide, which affects only about 7% of people.^[10] Prevalence varies significantly by region and ethnicity, with the highest rates observed in Europe and among Caucasian populations. In Western European countries, A- frequencies reach up to 7% or more; for example, it comprises 7.4% in Norway, 7% in Austria and Sweden, and 6.8% in France, based on national blood donor and genetic surveys.^[11] Among Caucasians more broadly, the rate hovers around 6-7%, contrasting sharply with lower incidences elsewhere due to historical genetic patterns.^[11] In Asia and Africa, A- is far less common, often below 1% of the population. Asian countries report rates of 0.1-0.3%, such as 0.25% in China, 0.2% in Japan, and 0.1% in South Korea and Thailand, according to blood bank records and population studies.^[11] Similarly, in African nations, the frequency is under 1%, with examples including 1.3% in Ghana, 0.3% in the Democratic Republic of Congo, and less than 1% in Nigeria, as documented in regional genetic surveys.^[11] These disparities highlight the influence of ancestral genetics on blood group distribution. Historical trends show minor shifts in A- prevalence influenced by migration and intermixing of populations, though changes remain subtle in most areas up to 2025. For instance, Australia's blood type profile has evolved with immigration over the past decade, decreasing the share of rarer Rh-negative types like A- due to influxes from regions with low Rh-negative prevalence.^[12] In contrast, Switzerland's distribution has stayed largely stable despite significant immigration since the mid-20th century, per longitudinal health data analyses.^[13] National blood donor databases and genetic studies continue to track these gradual adjustments globally.^[11]

Genetics and Inheritance

ABO System Genetics

The ABO blood group system is determined by a single gene located on the long arm of chromosome 9 at position 9q34.1-q34.2.^[2] This gene, known as ABO, encodes a glycosyltransferase enzyme that modifies the H antigen—a precursor carbohydrate structure present on the surface of red blood cells—by adding specific sugar residues to form the A or B antigens.^[2] The A allele specifically directs the addition of N-acetylgalactosamine to the H antigen, resulting in the expression of the A antigen.^[2] The ABO gene has three principal alleles: A, B, and O, which give rise to the four main blood types through their combinations.^[2] Individuals with blood type A possess the genotype AA or AO, where the A allele is expressed, leading to A antigen production on red blood cells.^[2] The A and B alleles exhibit codominance, meaning both are fully expressed in heterozygous individuals (resulting in AB blood type), while the O allele is recessive to both A and B.^[14] In AO heterozygotes, the single A allele is sufficient to produce the A antigen, as the O allele encodes a nonfunctional enzyme due to a frameshift mutation caused by a single nucleotide deletion at position 261.^[2] At the molecular level, the A and B alleles differ by seven nucleotide substitutions within the coding region, which result in four key amino acid changes: arginine to glycine at position 176 (R176G), glycine to serine at 235 (G235S), leucine to methionine at 266 (L266M), and glycine to alanine at 268 (G268A).^[2] These substitutions alter the enzyme's substrate specificity; the A variant preferentially binds N-acetylgalactosamine, while the B variant binds galactose, thereby determining the distinct antigenic structures.^[2] Numerous single nucleotide polymorphisms (SNPs) and other mutations in the A allele have been identified that can lead to variant A subgroups with reduced antigen expression, but the canonical A allele maintains robust A antigen synthesis in AA and AO genotypes.^[2]

Rh Factor Genetics

The negative Rh status characteristic of the A- blood type arises from the absence of the RhD antigen on the surface of red blood cells, which is encoded by the RHD gene located on the short arm of chromosome 1 at position 1p36.11-1p36.13.^[15] This absence occurs due to the lack of a functional RhD protein, most commonly resulting from a complete deletion of the RHD gene or disruptive mutations that prevent its expression.^[16] In individuals of European descent, who comprise a significant portion of those with A- blood, the predominant mechanism is a homozygous deletion of the RHD gene, arising from unequal crossing-over between flanking homologous sequences called Rhesus boxes.^[17] Other variants, such as point mutations or hybrid alleles, can also cause Rh negativity but are less frequent in this population.^[18] The Rh blood group system encompasses over 50 distinct antigens, though the D (RhD) antigen is the primary and most immunogenic one, serving as the key determinant of Rh-positive or Rh-negative status.^[8] Genotypically, Rh-negative individuals, including those with A- blood, are homozygous for the non-functional allele, denoted as rr (or dd in some notations), meaning they inherit the defective RHD variant from both parents.^[15] Heterozygous individuals (Rr) express the RhD antigen and are phenotypically Rh positive. The full A- phenotype integrates this Rh-negative genotype with the A antigen specificity from the ABO system.^[16] Inheritance of Rh negativity follows an autosomal recessive pattern, as the presence of even one functional RHD allele produces the dominant Rh-positive phenotype.^[15] Thus, both parents must contribute a non-functional allele for a child to be Rh negative. For instance, if both parents are heterozygous Rh positive (Rr), there is a 25% probability their offspring will be homozygous Rh negative (rr), a 50% chance of heterozygous Rh positive (Rr), and a 25% chance of homozygous Rh positive (RR).^[19] If both parents are Rh negative (rr), all offspring will inherit the rr genotype and be Rh negative.^[19] Ethnic variations in Rh-negative frequency reflect historical genetic drift and bottlenecks. The Basque population in northern Spain and southwestern France shows one of the highest global rates, reaching approximately 29%, linked to ancient population isolation that amplified the RHD deletion allele.^[20] In contrast, Rh negativity is rare in Asian populations (approximately 1%) and relatively low in African populations (1-8%), due to different mutational spectra like partial gene disruptions rather than full deletions.^[8]^[18]

Compatibility and Transfusion

Donor Compatibility

Individuals with A- blood type can donate whole blood to recipients with A- blood type, as the A antigens on red blood cells require ABO compatibility (A or AB recipients), but the anti-B antibodies in A- plasma necessitate recipients lacking B antigens (A or O), resulting in A- compatibility overall; the absence of Rh antigens and potential anti-Rh antibodies in the plasma necessitate matching to Rh-negative recipients to prevent hemolytic reactions.^[21] However, in practice, A- whole blood is often separated into components for broader use, with red blood cells suitable for A+ , A- , AB+ , and AB- recipients, since Rh-negative cells are compatible with Rh-positive individuals but conserved for Rh-negative patients to avoid alloimmunization.^[22] The American Red Cross emphasizes that A- red cells are particularly valuable for Rh-negative patients, who represent about 15% of the population and require negative blood to minimize sensitization risks.^[5] For plasma donation, A- individuals serve as compatible donors for A and O recipients (regardless of Rh status), because A-type plasma contains anti-B antibodies that do not react with A or O red cells, though it is not universal like AB plasma.^[23] This makes A- plasma useful in scenarios where type-specific or O-compatible plasma is needed, such as for trauma or surgical patients. The Rh factor does not affect plasma compatibility, as plasma lacks cellular antigens.^[24] Platelet donations from A- donors are generally compatible with A and AB recipients, with ABO matching preferred to reduce reactions, though platelets can often be transfused across minor incompatibilities due to their low antigen expression.^[25] Rh status is less critical for platelets, as alloimmunization risk is minimal, but A- platelets are in high demand for Rh-negative patients, including neonates and women of childbearing age.^[26] According to the American Red Cross, A- blood represents only about 6% of the U.S. population (1 in 16 people), yet it supports a significant portion of transfusion needs for A and AB Rh-negative individuals, underscoring the importance of these donors in maintaining supply for emergency and chronic care.^[21]

Recipient Compatibility

Individuals with A- blood type require careful matching for transfusions to avoid immune-mediated reactions, primarily due to the presence of A antigens on their red blood cells and absence of the RhD antigen. For whole blood transfusions, which are infrequently used in modern practice but follow the same principles as red cell components, A- recipients can only receive blood from A- or O- donors; this prevents agglutination from anti-A antibodies in non-A donor plasma and Rh sensitization from Rh-positive cells.^[27]^[25] Red blood cell transfusions for A- patients adhere to identical ABO and Rh rules, allowing receipt from A- or O- donors to ensure the transfused cells lack B antigens and the RhD antigen. In emergency situations where immediate transfusion is required and typed blood is unavailable, O- red cells serve as the universal donor option, compatible with all recipients including A-, though this is reserved to conserve O- supplies for Rh-negative patients.^[25]^[23] Plasma transfusions, which provide clotting factors and other proteins, follow reversed compatibility rules based on donor plasma antibodies interacting with recipient red cell antigens. A- recipients can receive plasma from A (positive or negative) or AB donors, as these types lack anti-A antibodies; AB plasma acts as a universal donor for plasma products, though A plasma is often preferred when available. Rh factor does not affect plasma compatibility, as plasma contains no red blood cell antigens.^[28]^[29]^[27] Pre-transfusion cross-matching is a critical procedure for all A- recipients, involving ABO and Rh typing, antibody screening, and a major cross-match to detect incompatibilities from minor antigens (e.g., Kell, Duffy). This testing ensures safe administration and mitigates risks such as delayed hemolytic transfusion reactions, which can occur 3–14 days post-transfusion if undetected alloantibodies target mismatched antigens, leading to extravascular hemolysis.^[30]^[31]

Medical and Health Aspects

Associated Health Risks

Individuals with A- blood type exhibit higher susceptibility to certain norovirus strains, as the A antigens on their red blood cells and mucosal surfaces serve as binding receptors for these pathogens. Specifically, strains like GII.4 preferentially attach to A antigens, enabling infection in secretor individuals who express these antigens; non-secretors lacking functional FUT2 enzyme are largely resistant. In challenge studies, approximately 70% of secretors (including those with type A) became infected with GII.4, compared to only 6% of non-secretors.^[32] A- blood type is associated with an elevated risk of venous thromboembolism (VTE), a cardiovascular condition involving blood clots in veins. Meta-analyses indicate that non-O blood types, including A, carry about an 80% higher relative risk of VTE compared to type O, attributed to elevated levels of von Willebrand factor and factor VIII in non-O individuals. This risk persists across subgroups, such as deep vein thrombosis (92% higher incidence) and unprovoked VTE.^[33]^[34] Regarding cancer, A- blood type correlates with increased odds of gastric and pancreatic cancers. A meta-analysis of case-control studies found that blood type A individuals have approximately 34% higher odds of gastric cancer compared to non-A types (OR = 1.34, 95% CI: 1.20-1.50), potentially linked to enhanced Helicobacter pylori adhesion to A antigens. For pancreatic cancer, type A is associated with a 40% elevated risk relative to type O (OR = 1.40, 95% CI: 1.32-1.49), with consistent findings across diverse populations.^[35]^[36] Early research on COVID-19 (2020-2023) suggested that A blood types faced slightly higher risks of infection and severe outcomes compared to type O, possibly due to viral interactions with A antigens on respiratory cells. However, Rh-negative status, as in A-, may confer minor protection against severe disease progression, with studies showing a 2-3% lower risk of intubation or death in Rh- individuals. These associations diminished in later analyses as other factors like vaccination influenced outcomes.^[37]^[38]^[39]

Pregnancy and Rh Incompatibility

Rh incompatibility arises when an Rh-negative mother, such as one with A- blood type, carries an Rh-positive fetus, leading to the potential production of maternal antibodies against fetal red blood cells. This condition, also known as Rh sensitization, typically occurs if fetal blood mixes with the mother's during pregnancy, delivery, miscarriage, or invasive procedures like amniocentesis, prompting the mother's immune system to form anti-D antibodies that can cross the placenta in subsequent pregnancies and attack the fetus's red blood cells.^[40]^[41]^[42] In the first pregnancy, the risk is low because sensitization usually happens at delivery, sparing the initial fetus; however, without intervention, up to 15% of subsequent Rh-positive pregnancies in sensitized Rh-negative mothers can result in hemolytic disease of the newborn (HDN), ranging from mild anemia to severe complications like hydrops fetalis, characterized by fetal heart failure, fluid accumulation, and organ enlargement. Newborns affected by HDN may exhibit severe jaundice, low muscle tone, lethargy, enlarged liver and spleen, or kernicterus—a dangerous buildup of bilirubin in the brain that can cause seizures, developmental delays, or death if untreated. For the mother, direct risks are minimal, but sensitization increases complications in future pregnancies. Approximately 15% of women worldwide are Rh-negative, heightening the relevance for A- individuals.^[40]^[42]^[41] Diagnosis involves early prenatal blood tests to determine Rh status and antibody screening; if antibodies are detected, further monitoring includes ultrasounds to assess fetal anemia or fluid buildup, amniocentesis for bilirubin levels in amniotic fluid, or percutaneous umbilical blood sampling. In severe cases, intrauterine blood transfusions via the umbilical cord can treat fetal anemia, often requiring multiple procedures and potentially early delivery. Postnatally, affected infants receive phototherapy to break down bilirubin, intravenous immunoglobulin, or exchange transfusions to remove damaged red blood cells.^[40]^[42]^[41] Prevention has dramatically reduced Rh incompatibility since the introduction of RhoGAM (Rh immunoglobulin), a prophylactic injection given to Rh-negative mothers at 28 weeks of gestation and within 72 hours postpartum if the infant is Rh-positive, which neutralizes any fetal Rh-positive cells in the mother's blood and prevents sensitization in about 99% of cases. Routine administration during pregnancy does not clearly reduce alloimmunization rates based on low-quality evidence from randomized trials, but it significantly lowers risks in future pregnancies; no serious adverse effects are associated with RhoGAM, though theoretical risks of blood-borne transmission exist. All Rh-negative pregnant women, including those with A- blood, should receive this standard care to avoid preventable outcomes.^[40]^[43]^[41]

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