What you carry at this position in your DNA and what research says about it.
Immune and Drug Sensitivity: 6/10 evidence, 31 publications.
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Sample genotype (not yours): T/T
Typical Immune Response and Drug Sensitivity
You carry two copies of the common T allele. This results in standard baseline risks for autoimmune skin conditions and typical drug tolerance.
What this genotype means: Typical risk of psoriasis; Standard tolerance to flucloxacillin and abacavir; Typical baseline HIV progression rate.
Sample genotype (not yours): G/G
Strong HIV Protection with Maximum Drug Risks
Carrying two G alleles offers robust natural defense against HIV progression but carries very high risks for psoriasis and severe drug toxicities.
What this genotype means: Highly optimized natural immune control of HIV replication; Significantly elevated risk of psoriasis; Extreme risk of severe adverse reactions to flucloxacillin and abacavir.
Sample genotype (not yours): T/G
Slower HIV Progression but Higher Drug Risks
Carrying one G allele provides natural protection against HIV progression but significantly increases your risk for psoriasis and severe drug reactions.
What this genotype means: Slower progression and lower viral load if infected with HIV; Approximately 4x higher risk of developing psoriasis; Greatly increased risk of severe allergic reactions to abacavir and flucloxacillin.
Gene function and biological role
Gene Function: The HCP5 gene, located within the major histocompatibility complex on chromosome 6, encodes a non-coding RNA that is highly polymorphic [1]. This gene is situated very close to the HLA-B gene, which plays a central role in how the immune system recognizes foreign pathogens [2]. Because of this close physical proximity, specific variations in HCP5 are almost always inherited alongside particular HLA-B tissue types [3]. Consequently, HCP5 serves as an exceptionally strong genetic proxy for immune-related traits and drug reactions driven by the HLA region [4].
Variant Impact: The rs2395029 variant is a single nucleotide change in the HCP5 gene where the common T allele is replaced by the G allele. This genetic change is in near-perfect linkage disequilibrium with the HLA-B*5701 immune system allele in populations of European and Hispanic ancestry [3]. Because of this tight genetic link, carrying the G allele serves as an accurate marker for several distinct immune phenotypes [4]. These include a significantly lower viral set point during HIV infection, but also a greatly elevated risk of severe hypersensitivity reactions to specific medications [1] [5].
Key Insight: The same genetic variant that provides powerful natural protection against HIV progression also dramatically increases the risk of life-threatening allergic reactions to common antibiotics and antiviral medications.
Location: HCP5. Chromosome 6 · 6p21.33 · 31.5 Mb
Estimated prevalence by population
Global 95.2%; European 92.8%; African 98.5%; East Asian 98.3%; South Asian 90.6%; Americas 97.2%; Ashkenazi 91.6%; Finnish 98.1%; Middle Eastern 94.0%; Amish 71.8%.
Estimated TT genotype frequency.
Global 4.8%; European 7.1%; African 1.5%; East Asian 1.7%; South Asian 9.2%; Americas 2.7%; Ashkenazi 8.2%; Finnish 1.8%; Middle Eastern 5.9%; Amish 25.8%.
Estimated TG genotype frequency.
Global 0.1%; European 0.1%; African < 0.1%; East Asian < 0.1%; South Asian 0.2%; Americas < 0.1%; Ashkenazi 0.2%; Finnish < 0.1%; Middle Eastern 0.1%; Amish 2.3%.
Estimated GG genotype frequency.
Showing effects for T/T genotype
Immunity & Inflammation
Infection Susceptibility & Resistance
HIV Progression Rate. Evidence: 6/10. Source: PMID 19115949. Typical Progression.
Organ Systems
Skin & Hair Conditions
Psoriasis. Evidence: 4/10. Source: PMID 18369459. Typical Risk.
Pharmacogenomics
Antimicrobial & Antiviral Response
Flucloxacillin Toxicity. Evidence: 6/10. Source: PMID 19483685. Typical Risk.
Abacavir Sensitivity. Evidence: 4/10. Source: PMID 18684101. Typical Response.
Showing effects for G/G genotype
HIV Progression Rate. Evidence: 6/10. Source: PMID 19115949. Slower Progression.
Psoriasis. Evidence: 4/10. Source: PMID 18369459. ~4x Increased Risk.
Flucloxacillin Toxicity. Evidence: 6/10. Source: PMID 19483685. Extreme Liver Risk.
Abacavir Sensitivity. Evidence: 4/10. Source: PMID 18684101. High Allergy Risk.
Showing effects for T/G genotype
Flucloxacillin Toxicity. Evidence: 6/10. Source: PMID 19483685. High Liver Risk.
What this genotype means for the people who carry it
Sample genotype: TT (Homozygous)
Most individuals globally carry the T/T genotype, which represents the standard baseline for immune system behavior at this locus. Because you do not carry the G allele, you have a typical risk profile for developing the autoimmune skin condition psoriasis [1]. Furthermore, you lack the genetic marker most strongly associated with severe liver injury when taking the antibiotic flucloxacillin [2]. Your body is also expected to tolerate the antiviral drug abacavir normally, without the high risk of systemic hypersensitivity reactions seen in G allele carriers [3]. However, you do not possess the specific genetic advantage that helps the immune system naturally suppress HIV replication and delay progression to AIDS [4].
Typical risk of psoriasis; Standard tolerance to flucloxacillin and abacavir; Typical baseline HIV progression rate.
Sample genotype: GG (Homozygous)
This rare genotype maximizes both the immunological benefits and the clinical risks associated with this locus. Carrying two copies of the G allele strongly correlates with the HLA-B*5701 tissue type, making you highly likely to naturally control HIV replication and experience exceptionally slow disease progression [1]. On the other hand, this genetic profile is associated with a fourfold increase in your baseline risk for psoriasis [2]. It also places you at extreme risk for severe liver toxicity if you take the antibiotic flucloxacillin [3]. Furthermore, exposure to the antiviral drug abacavir is highly likely to trigger a dangerous, multi-organ hypersensitivity reaction due to your genetic profile [4].
Highly optimized natural immune control of HIV replication; Significantly elevated risk of psoriasis; Extreme risk of severe adverse reactions to flucloxacillin and abacavir.
Sample genotype: TG (Heterozygous)
This genotype represents a major evolutionary trade-off in immune system function. Having one copy of the G allele means you likely carry the HLA-B*5701 tissue type, which is highly protective against HIV progression [1]. If exposed to HIV, your immune system is genetically primed to maintain a lower viral load and delay the onset of AIDS [2]. However, this heightened immune state increases your risk of developing psoriasis by approximately fourfold [3]. Additionally, you face a significantly elevated risk of drug-induced liver injury if prescribed the antibiotic flucloxacillin, and a high risk of a severe, potentially life-threatening allergic reaction to the antiviral drug abacavir [4] [5].
Slower progression and lower viral load if infected with HIV; Approximately 4x higher risk of developing psoriasis; Greatly increased risk of severe allergic reactions to abacavir and flucloxacillin.
Variants with shared genetic architecture
rs10484554 · HLA-C Gene · Chr 6 · Psoriasis Risk
rs11209026 · IL23R Gene · Chr 1 · Autoimmune Disease Risk
rs11795343 · DDX58 Gene · Chr 9 · Psoriasis Risk
The major genetic determinants of HIV-1 control affect HLA class I peptide presentation.
HLA-B*5701 genotype is a major determinant of drug-induced liver injury due to flucloxacillin.
A genome-wide association study of psoriasis and psoriatic arthritis identifies new disease loci.
Common genetic variation and the control of HIV-1 in humans.
Content updated August 2026.
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