What you carry at this position in your DNA and what research says about it.
Viral Control and Crohn's: 6/10 evidence, 25 publications.
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Sample genotype (not yours): T/T
Typical Viral Control and Crohn's Disease Risk
Typical levels of HLA-C expression result in standard viral clearance rates. There is no elevated risk for Crohn's disease associated with this genotype.
What this genotype means: Typical viral clearance rates; Baseline risk for Crohn's disease.
Sample genotype (not yours): C/C
Maximum Viral Control with Higher Crohn's Risk
High HLA-C expression significantly reduces viral loads during infection. This strong viral defense is offset by a higher risk of developing Crohn's disease.
What this genotype means: Approximately 90% reduction in HIV viral load; Elevated risk of Crohn's disease; Enhanced protection against Hepatitis C.
Sample genotype (not yours): T/C
Enhanced Viral Control with Slightly Higher Crohn's Risk
A moderate increase in HLA-C expression helps reduce viral loads during infection. This immune boost comes with a slightly increased risk of developing Crohn's disease.
What this genotype means: Approximately 60% reduction in HIV viral load; Slightly increased risk of Crohn's disease; Improved protection against Hepatitis C.
Gene function and biological role
Gene Function: The genomic region upstream of the HLA-C gene plays a critical role in regulating the human immune system's response to viral infections [1]. HLA-C encodes a major histocompatibility complex class I heavy chain receptor that presents intracellular antigens to cytotoxic T cells [2]. Higher expression of this receptor on cell surfaces enhances the immune system's ability to recognize and destroy virus-infected cells [2]. Conversely, lower expression levels can allow viruses to evade immune detection and replicate more freely [3]. This regulatory region is heavily studied for its impact on chronic viral infections and autoimmune susceptibility [1] [4].
Variant Impact: This single nucleotide polymorphism is located approximately 35 kilobases upstream of the HLA-C gene and acts as a major regulator of its expression [1]. The genetic variation directly influences how much HLA-C protein is presented on the surface of immune cells [3]. Higher cell-surface expression associated with the variant helps the body control viral replication, particularly during HIV infection [1] [5]. However, the same increased immune activity is also linked to a higher risk of inflammatory conditions like Crohn's disease [6]. This dual effect makes the variant a key focus of research into the evolutionary trade-offs of human immunity [1] [6].
Key Insight: A single genetic letter change can reduce HIV viral load by up to 90 percent, but this powerful defense mechanism simultaneously increases the risk of developing Crohn's disease.
Location: HLA-C. Chromosome 6 · 6p21.33 · 31.3 Mb
Estimated prevalence by population
Global 43.4%; European 41.1%; African 48.5%; East Asian 36.7%; South Asian 24.2%; Americas 47.6%; Ashkenazi 17.6%; Finnish 53.1%; Middle Eastern 36.2%; Amish 35.2%.
Estimated TT genotype frequency.
Global 44.5%; European 46.0%; African 42.3%; East Asian 47.8%; South Asian 50.0%; Americas 42.8%; Ashkenazi 48.7%; Finnish 39.5%; Middle Eastern 47.9%; Amish 48.3%.
Estimated TC genotype frequency.
Global 12.2%; European 12.9%; African 9.2%; East Asian 15.5%; South Asian 25.8%; Americas 9.6%; Ashkenazi 33.7%; Finnish 7.3%; Middle Eastern 15.8%; Amish 16.5%.
Estimated CC genotype frequency.
Showing effects for T/T genotype
Immunity & Inflammation
Infection Susceptibility & Resistance
HIV Control. Evidence: 5/10. Source: PMID 20041166. Typical Control.
Hepatitis C Clearance. Evidence: 3/10. Source: PMID 30102364. Typical Protection.
Chronic Inflammatory Diseases
Crohn's Disease. Evidence: 6/10. Source: PMID 23128233. Typical Risk.
Inflammatory & Circulating Protein Markers
HLA-C Expression. Evidence: 4/10. Source: PMID 19935663. Typical Expression.
Showing effects for C/C genotype
HIV Control. Evidence: 5/10. Source: PMID 20041166. ~90% Reduction.
Hepatitis C Clearance. Evidence: 3/10. Source: PMID 30102364. Increased Protection.
Crohn's Disease. Evidence: 6/10. Source: PMID 23128233. ~1.15x Risk.
HLA-C Expression. Evidence: 4/10. Source: PMID 19935663. Highly Increased.
Showing effects for T/C genotype
HIV Control. Evidence: 5/10. Source: PMID 20041166. ~60% Reduction.
HLA-C Expression. Evidence: 4/10. Source: PMID 19935663. Increased Expression.
What this genotype means for the people who carry it
Sample genotype: TT (Homozygous)
Standard levels of HLA-C expression are maintained with this genotype, representing the baseline immune profile of the general population [1]. Without the elevated receptor expression of the alternative variant, the immune system clears viral pathogens at a typical rate [1] [2]. This means there is no genetic reduction in viral load during chronic infections like HIV [2]. However, the lower baseline immune activation also means there is no increased susceptibility to autoimmune disorders like Crohn's disease [3]. Research shows that individuals with this genotype maintain a typical risk profile for inflammatory bowel diseases [3] [4]. It represents the most common genetic baseline across many global ancestries.
Typical viral clearance rates; Baseline risk for Crohn's disease.
Sample genotype: CC (Homozygous)
Maximum levels of HLA-C surface expression are promoted by carrying two copies of the protective allele [1]. This high density of receptors allows the immune system to aggressively target and destroy virus-infected cells [2]. Clinical cohorts show that this genotype is associated with an average 90% reduction in HIV viral load [3]. It also significantly increases the probability of remaining seronegative when exposed to Hepatitis C [4]. The trade-off for this powerful viral defense is a significantly higher susceptibility to autoimmune inflammation [5]. The risk of developing Crohn's disease is increased by approximately 15% compared to the baseline genotype [5] [6]. This represents a classic evolutionary trade-off between infectious disease defense and autoimmune risk.
Approximately 90% reduction in HIV viral load; Elevated risk of Crohn's disease; Enhanced protection against Hepatitis C.
Sample genotype: TC (Heterozygous)
A moderate increase in HLA-C surface expression is driven by carrying one copy of the protective allele [1]. This elevated expression enhances the presentation of viral antigens to cytotoxic T cells, helping the body control viral replication [2]. Studies indicate that this genotype is associated with an average 60% reduction in HIV viral load during infection [3]. Additionally, it provides a protective effect against other viral exposures, such as increasing the likelihood of remaining seronegative for Hepatitis C [4]. However, the heightened immune surveillance slightly increases the risk of inflammatory bowel diseases [5]. The odds of developing Crohn's disease are slightly elevated due to this increased immune reactivity [5] [6].
Approximately 60% reduction in HIV viral load; Slightly increased risk of Crohn's disease; Improved protection against Hepatitis C.
Variants with shared genetic architecture
rs10484554 · HLA-C Gene · Chr 6 · Psoriasis Risk
rs12191877 · HLA-C Gene · Chr 6 · Psoriasis Risk
rs2542151 · PTPN2 Gene · Chr 18 · Autoimmune Disease Risk
Common genetic variation and the control of HIV-1 in humans.
The major genetic determinants of HIV-1 control affect HLA class I peptide presentation.
HLA-C cell surface expression and control of HIV/AIDS correlate with a variant upstream of HLA-C.
Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease.
Content updated August 2026.
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