What you carry at this position in your DNA and what research says about it.
Duffy Blood Group: 7/10 evidence, 36 publications.
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Sample genotype (not yours): G/G
Duffy Fy(a+b-) Type and Lower Malaria Risk
Red blood cells express only the Fya antigen, which provides significant protection against certain types of malaria. This blood group profile is also linked to lower circulating levels of several inflammatory chemokines.
What this genotype means: Duffy Fy(a+b-) blood group phenotype; Reduced risk of clinical Plasmodium vivax malaria; Lower circulating levels of inflammatory chemokines.
Sample genotype (not yours): A/A
Duffy Fy(a-b+) Type and Higher Malaria Risk
Red blood cells express only the Fyb antigen, which is highly compatible with malaria parasite binding. This profile is also associated with higher circulating levels of inflammatory chemokines.
What this genotype means: Duffy Fy(a-b+) blood group phenotype; Increased susceptibility to Plasmodium vivax malaria; Higher circulating levels of inflammatory chemokines.
Sample genotype (not yours): G/A
Duffy Fy(a+b+) Type and Typical Malaria Risk
Red blood cells express both Fya and Fyb antigens, resulting in a typical susceptibility to malaria. This co-dominant profile leads to intermediate levels of circulating inflammatory chemokines.
What this genotype means: Duffy Fy(a+b+) blood group phenotype; Typical susceptibility to Plasmodium vivax malaria; Intermediate circulating levels of inflammatory chemokines.
Gene function and biological role
Gene Function: The ACKR1 gene, formerly known as DARC, encodes the atypical chemokine receptor 1 protein, which is expressed on red blood cells and endothelial cells [1]. This protein serves as a critical receptor for several inflammatory chemokines, acting as a buffer or sink to regulate their levels in the bloodstream [2]. It also functions as the primary gateway that certain malaria parasites use to invade red blood cells [2]. Variations in this gene directly determine Duffy blood group antigens, which are vital for blood transfusion compatibility [3].
Variant Impact: The rs12075 variant is a missense mutation in the ACKR1 gene that changes the amino acid at position 42 from glycine to aspartic acid [3]. This single nucleotide change alters the structure of the extracellular domain of the Duffy protein, creating two distinct antigens known as Fya and Fyb [3]. The G allele encodes the Fya antigen, while the A allele encodes the Fyb antigen [1]. This structural change significantly impacts how the receptor binds to both inflammatory chemokines and malaria parasites [2].
Read on the Duffy Blood Group page
Key Insight: This variant determines your Duffy blood group type, which directly influences your susceptibility to certain malaria parasites and regulates circulating levels of key inflammatory proteins.
Location: ACKR1. Chromosome 1 · 1q23.2 · 159.2 Mb
Origin Story: The Duffy blood group system has undergone intense evolutionary pressure, particularly in regions where malaria is endemic, as the absence or alteration of these antigens prevents the malaria parasite from entering red blood cells.
Estimated prevalence by population
Global 16.8%; European 17.7%; African 0.6%; East Asian 87.7%; South Asian 38.9%; Americas 18.8%; Ashkenazi 19.2%; Finnish 25.1%; Middle Eastern 11.3%; Amish 26.5%.
Estimated GG genotype frequency.
Global 38.0%; European 48.8%; African 14.2%; East Asian 11.9%; South Asian 46.9%; Americas 49.1%; Ashkenazi 49.2%; Finnish 50.0%; Middle Eastern 44.6%; Amish 50.0%.
Estimated GA genotype frequency.
Global 45.2%; European 33.5%; African 85.2%; East Asian 0.4%; South Asian 14.2%; Americas 32.0%; Ashkenazi 31.5%; Finnish 24.9%; Middle Eastern 44.1%; Amish 23.6%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Cardiovascular & Metabolic
Blood Cell & Iron Traits
Duffy Blood Group. Evidence: 7/10. Source: PMID 7705836. Fy(a+b-).
White Blood Cell Count. Evidence: 10/10. Source: PMID 32888494. Typical.
Immunity & Inflammation
Infection Susceptibility & Resistance
Malaria Susceptibility. Evidence: 3/10. Source: PMID 10791881. Lower Risk.
Inflammatory & Circulating Protein Markers
MCP-1 Levels. Evidence: 4/10. Source: PMID 23017229. Lower Levels.
Organ Systems
Liver Function & Disease
Hepatitis C Fibrosis Risk. Evidence: 3/10. Source: PMID 30970632. Lower Risk.
Showing effects for A/A genotype
Duffy Blood Group. Evidence: 7/10. Source: PMID 7705836. Fy(a-b+).
White Blood Cell Count. Evidence: 10/10. Source: PMID 32888494. Slightly Higher.
Malaria Susceptibility. Evidence: 3/10. Source: PMID 10791881. Higher Risk.
MCP-1 Levels. Evidence: 4/10. Source: PMID 23017229. Higher Levels.
Hepatitis C Fibrosis Risk. Evidence: 3/10. Source: PMID 30970632. Higher Risk.
Showing effects for G/A genotype
Duffy Blood Group. Evidence: 7/10. Source: PMID 7705836. Fy(a+b+).
Malaria Susceptibility. Evidence: 3/10. Source: PMID 10791881. Typical Risk.
MCP-1 Levels. Evidence: 4/10. Source: PMID 23017229. Intermediate Levels.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Erythrocytes with this genetic profile display the Fya antigen on their surface, corresponding to the Duffy Fy(a+b-) phenotype [1]. This specific molecular structure makes it much harder for the Plasmodium vivax malaria parasite to bind to and invade red blood cells [2]. Studies show that this phenotype is associated with a 30% to 80% reduced risk of clinical vivax malaria [2]. Additionally, this configuration alters the receptor's chemokine-buffering capacity, resulting in lower circulating levels of inflammatory proteins like MCP-1 [3]. In the context of chronic hepatitis C infection, carrying at least one G allele is associated with a lower risk of liver fibrosis progression and cirrhosis [4].
Duffy Fy(a+b-) blood group phenotype; Reduced risk of clinical Plasmodium vivax malaria; Lower circulating levels of inflammatory chemokines.
Sample genotype: AA (Homozygous)
Erythrocytes with this genetic profile express only the Fyb antigen, corresponding to the Duffy Fy(a-b+) phenotype [1]. This specific molecular structure is highly compatible with the Duffy binding protein of the Plasmodium vivax malaria parasite, facilitating efficient cell invasion [2]. Consequently, this phenotype carries a higher susceptibility to clinical vivax malaria compared to those carrying the G allele [2]. This configuration also leads to significantly higher circulating levels of inflammatory chemokines, particularly MCP-1, as the receptor binds and clears these proteins differently [3]. Furthermore, in patients with chronic hepatitis C, this genotype is associated with a higher risk of liver stiffness and accelerated progression toward cirrhosis [4].
Duffy Fy(a-b+) blood group phenotype; Increased susceptibility to Plasmodium vivax malaria; Higher circulating levels of inflammatory chemokines.
Sample genotype: GA (Heterozygous)
Erythrocytes with this heterozygous profile express both the Fya and Fyb antigens, resulting in the Duffy Fy(a+b+) phenotype [1]. Because both antigens are present, the Plasmodium vivax malaria parasite can readily utilize the Fyb antigen to bind and enter red blood cells, leading to a typical risk of infection [2]. This co-dominant expression also results in intermediate circulating levels of various inflammatory chemokines, such as MCP-1 and interleukin-8 [3]. However, the presence of the G allele still offers some protective benefits in other inflammatory contexts. For instance, patients with this genotype who have chronic hepatitis C show a reduced risk of liver stiffness and fibrosis progression compared to those with the AA genotype [4].
Duffy Fy(a+b+) blood group phenotype; Typical susceptibility to Plasmodium vivax malaria; Intermediate circulating levels of inflammatory chemokines.
Variants with shared genetic architecture
rs2814778 · ACKR1 Gene · Chr 1 · Duffy Blood Group and Immunity
rs34599082 · ACKR1 Gene · Chr 1 · Duffy Blood Group
rs2228467 · ACKR2 Gene · Chr 3 · Inflammation Risk
The Duffy protein: a malarial and chemokine receptor.
Molecular basis and PCR-DNA typing of the Fya/fyb blood group polymorphism.
Content updated August 2026.
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