What you carry at this position in your DNA and what research says about it.
Hepatitis C Treatment Response: 9/10 evidence, 89 publications.
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Sample genotype (not yours): T/T
Excellent Hepatitis C Treatment Response
A highly favorable response to hepatitis C treatments and a higher rate of spontaneous viral clearance characterize this profile. However, it may carry a slightly higher risk of developing cryoglobulinemia during specific interferon therapies.
What this genotype means: Highly favorable response to hepatitis C antiviral therapies; Increased likelihood of spontaneous viral clearance; Slightly higher risk of treatment-related cryoglobulinemia.
Sample genotype (not yours): G/G
Poor Hepatitis C Treatment Response
A significantly lower response rate to standard hepatitis C treatments and a higher risk of chronic infection are common with this profile. It also increases the risk of elevated cholesterol during antiviral therapy.
What this genotype means: Significantly lower response to standard hepatitis C therapies; Highest risk of chronic hepatitis C infection; Increased risk of high cholesterol during antiviral therapy.
Sample genotype (not yours): T/G
Reduced Hepatitis C Treatment Response
A moderately lower response rate to standard hepatitis C treatments and a higher risk of chronic infection are linked to this profile. It is also associated with a higher risk of elevated cholesterol during certain antiviral therapies.
What this genotype means: Moderately lower response to hepatitis C treatments; Higher likelihood of chronic hepatitis C infection; Increased risk of high cholesterol during antiviral therapy.
Gene function and biological role
Gene Function: The IFNL3 gene, also known as IL28B, encodes interferon lambda-3, a type III interferon cytokine that plays a critical role in the innate immune response against viral infections [1]. It is located on chromosome 19 alongside other type III interferons like IFNL1 and IFNL2 [2]. This cytokine acts through the JAK-STAT pathway to trigger an antiviral cascade that helps clear viral pathogens from host cells [1]. Variations in this gene are among the most powerful predictors of whether a person can naturally clear the hepatitis C virus or respond successfully to interferon-based therapies [3].
Variant Impact: The rs8099917 variant is an intergenic single nucleotide polymorphism located near the IFNL3 gene on chromosome 19. This genetic change influences the expression of interferon-stimulated genes in the liver, which directly impacts the body's ability to fight off viral infections [4]. The major T allele is highly favorable, promoting natural clearance of the hepatitis C virus and a robust response to antiviral medications [1]. Conversely, the minor G allele is associated with a reduced ability to clear the virus and a significantly lower rate of responding to interferon-based treatments [2].
Key Insight: This genetic variant is one of the strongest known predictors of response to hepatitis C treatment, sometimes outweighing clinical markers like viral load or liver damage.
Location: IFNL3. Chromosome 19 · 19q13.2 · 39.3 Mb
Estimated prevalence by population
Global 71.6%; European 64.9%; African 86.8%; East Asian 87.3%; South Asian 71.7%; Americas 55.0%; Ashkenazi 63.3%; Finnish 75.8%; Middle Eastern 58.0%; Amish 64.2%.
Estimated TT genotype frequency.
Global 25.6%; European 31.4%; African 12.7%; East Asian 12.2%; South Asian 25.9%; Americas 38.3%; Ashkenazi 32.5%; Finnish 22.5%; Middle Eastern 36.3%; Amish 31.8%.
Estimated TG genotype frequency.
Global 2.9%; European 3.8%; African 0.5%; East Asian 0.4%; South Asian 2.3%; Americas 6.7%; Ashkenazi 4.2%; Finnish 1.7%; Middle Eastern 5.7%; Amish 3.9%.
Estimated GG genotype frequency.
Showing effects for T/T genotype
Pharmacogenomics
Drug Metabolism Enzyme Activity
Treatment Response. Evidence: 9/10. Source: PMID 19749757. Excellent Response.
Immunity & Inflammation
Infection Susceptibility & Resistance
Chronic Infection Risk. Evidence: 9/10. Source: PMID 19749757. Lower Risk.
Autoimmune Diseases
Cryoglobulinemia. Evidence: 6/10. Source: PMID 28453396. Increased Risk.
Cardiovascular & Metabolic
Lipids & Cholesterol
Cholesterol Levels. Evidence: 5/10. Source: PMID 31144350. Typical Levels.
Showing effects for G/G genotype
Treatment Response. Evidence: 9/10. Source: PMID 19749757. Poor Response.
Chronic Infection Risk. Evidence: 9/10. Source: PMID 19749757. Higher Risk.
Cryoglobulinemia. Evidence: 6/10. Source: PMID 28453396. Lower Risk.
Cholesterol Levels. Evidence: 5/10. Source: PMID 31144350. Increased Risk.
Showing effects for T/G genotype
Treatment Response. Evidence: 9/10. Source: PMID 19749757. Reduced Response.
Chronic Infection Risk. Evidence: 9/10. Source: PMID 19749757. Increased Risk.
What this genotype means for the people who carry it
Sample genotype: TT (Homozygous)
The presence of two T alleles is the most common genetic profile globally and is highly advantageous for viral defense. Research shows that individuals with this genotype are significantly more likely to naturally clear the hepatitis C virus without intervention [1]. If treatment is required, they exhibit an excellent response rate to pegylated interferon and ribavirin therapies [2]. This genotype is also linked to a lower risk of chronic hepatitis C infection overall [3]. However, some studies note a slightly increased likelihood of developing cryoglobulinemia, an inflammatory vascular condition, during interferon-based treatments [4].
Highly favorable response to hepatitis C antiviral therapies; Increased likelihood of spontaneous viral clearance; Slightly higher risk of treatment-related cryoglobulinemia.
Sample genotype: GG (Homozygous)
Two copies of the G allele are associated with the lowest rates of spontaneous hepatitis C clearance and treatment response. Individuals with this genotype have a significantly higher risk of developing chronic hepatitis C after exposure [1]. Standard treatments using pegylated interferon and ribavirin are much less effective for this group, often requiring alternative or intensified therapeutic strategies [2]. Furthermore, modern direct-acting antiviral treatments are linked to a higher risk of developing elevated low-density lipoprotein cholesterol in G/G carriers [3]. However, they benefit from a lower risk of developing cryoglobulinemia during interferon therapy [4].
Significantly lower response to standard hepatitis C therapies; Highest risk of chronic hepatitis C infection; Increased risk of high cholesterol during antiviral therapy.
Sample genotype: TG (Heterozygous)
A single copy of the G allele moderately reduces the body's natural ability to clear the hepatitis C virus. Clinical studies indicate that individuals with this genotype have lower odds of achieving a sustained virological response when treated with pegylated interferon and ribavirin [1]. They also face a higher risk of the infection transitioning into a chronic state [2]. Additionally, during treatment with modern direct-acting antivirals, this genotype is associated with an increased risk of developing high cholesterol [3]. On the positive side, they have a lower risk of interferon-induced cryoglobulinemia compared to those with the T/T genotype [4].
Moderately lower response to hepatitis C treatments; Higher likelihood of chronic hepatitis C infection; Increased risk of high cholesterol during antiviral therapy.
Variants with shared genetic architecture
rs11881222 · IFNL3 Gene · Chr 19 · Hepatitis C Clearance
rs12980275 · IFNL3 Gene · Chr 19 · Viral Defense and Sleep
rs8105790 · IFNL3 Gene · Chr 19 · Hepatitis Viral Clearance
IL28B is associated with response to chronic hepatitis C interferon-alpha and ribavirin therapy.
Pharmacogenetic analysis of hepatitis C virus related mixed cryoglobulinemia.
Content updated August 2026.
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