What you carry at this position in your DNA and what research says about it.
Lung Fibrosis Risk: 10/10 evidence, 29 publications.
You're viewing every possible genotype for this variant.
None of these is your result. Use the genotype toggle to compare them, then sign up and upload your DNA to see which one is yours.
Sample genotype (not yours): G/G
Typical Lung Fibrosis Risk
A typical baseline risk for progressive lung scarring is expected with this common genetic profile. There may be a very slightly higher susceptibility to severe COVID-19 symptoms compared to T allele carriers.
What this genotype means: Typical baseline risk of pulmonary fibrosis; Slightly higher susceptibility to severe COVID-19.
Sample genotype (not yours): G/T
Moderately Higher Lung Fibrosis Risk
A moderately higher risk of developing progressive lung scarring is associated with this genetic profile. This variant leads to increased mucus production in the deep airways of the lungs.
What this genotype means: Moderately increased risk of pulmonary fibrosis; Slightly lower susceptibility to severe COVID-19.
Sample genotype (not yours): T/T
Significantly Higher Lung Fibrosis Risk
A highly elevated risk of developing progressive lung scarring is associated with this genetic profile. This genotype leads to substantial overproduction of mucus in the deep lung tissue.
What this genotype means: Highly increased risk of pulmonary fibrosis; Substantially higher mucin 5B protein levels in the lungs.
Gene function and biological role
Gene Function: The MUC5B gene encodes mucin 5B, a major gel-forming glycoprotein in mucus [1]. This protein plays a vital role in lubricating airways and clearing out inhaled pathogens and particles [1]. However, abnormal production of mucin 5B can disrupt the delicate lining of the lungs [2]. Over time, this disruption can lead to chronic irritation, microscopic injuries, and progressive scarring of lung tissue [2].
Variant Impact: The rs35705950 variant is located in the promoter region of the MUC5B gene, which acts as a control switch for gene activity [1]. Carrying the T allele significantly increases the transcription and production of mucin 5B in the deep airways [1]. This excess mucus is thought to impair the lungs' natural self-cleaning mechanism, leading to chronic cellular stress [2]. Over time, this persistent stress triggers a fibrotic healing response, causing healthy lung tissue to be replaced by stiff scar tissue [2].
Key Insight: This single genetic variant is the strongest known genetic risk factor for developing idiopathic pulmonary fibrosis, yet carrying it does not guarantee you will get the disease.
Location: MUC5B. Chromosome 11 · 11p15.5 · 1.2 Mb
Estimated prevalence by population
Global 84.9%; European 79.2%; African 95.9%; East Asian 98.6%; South Asian 83.7%; Americas 83.7%; Ashkenazi 77.9%; Finnish 78.3%; Middle Eastern 75.2%; Amish 73.0%.
Estimated GG genotype frequency.
Global 14.3%; European 19.6%; African 4.0%; East Asian 1.4%; South Asian 15.5%; Americas 15.6%; Ashkenazi 20.7%; Finnish 20.3%; Middle Eastern 23.0%; Amish 24.9%.
Estimated GT genotype frequency.
Global 0.8%; European 1.2%; African < 0.1%; East Asian < 0.1%; South Asian 0.7%; Americas 0.7%; Ashkenazi 1.4%; Finnish 1.3%; Middle Eastern 1.8%; Amish 2.1%.
Estimated TT genotype frequency.
Showing effects for G/G genotype
Organ Systems
Respiratory Health
Pulmonary Fibrosis. Evidence: 10/10. Source: PMID 21506748. Typical Risk.
Lung Disease. Evidence: 10/10. Source: PMID 23692170. Typical Risk.
Immunity & Inflammation
Infection Susceptibility & Resistance
COVID-19 Severity. Evidence: 8/10. Source: PMID 35922517. Slightly Higher Risk.
Cardiovascular & Metabolic
Blood Cell & Iron Traits
White Blood Cell Count. Evidence: 8/10. Source: PMID 39024449. Typical.
Showing effects for G/T genotype
Pulmonary Fibrosis. Evidence: 10/10. Source: PMID 21506748. ~5x to 9x Risk.
Lung Disease. Evidence: 10/10. Source: PMID 23692170. Increased Risk.
COVID-19 Severity. Evidence: 8/10. Source: PMID 35922517. Typical Risk.
White Blood Cell Count. Evidence: 8/10. Source: PMID 39024449. Slightly Higher.
Showing effects for T/T genotype
Pulmonary Fibrosis. Evidence: 10/10. Source: PMID 21506748. ~10x to 20x Risk.
Lung Disease. Evidence: 10/10. Source: PMID 23692170. Highly Increased Risk.
COVID-19 Severity. Evidence: 8/10. Source: PMID 35922517. Slightly Lower Risk.
White Blood Cell Count. Evidence: 8/10. Source: PMID 39024449. Higher.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
The G/G genotype represents the most common genetic profile globally, occurring in over 90% of the population [1]. Normal, baseline levels of mucin 5B protein production in the lungs are typical for this profile [1]. Because the T risk allele is absent, the risk of developing idiopathic pulmonary fibrosis or other interstitial lung diseases is not genetically elevated [2]. However, some studies suggest that the G allele is associated with a very slight increase in susceptibility to severe COVID-19 hospitalization [3]. Overall, this lung health profile is considered typical [2].
Typical baseline risk of pulmonary fibrosis; Slightly higher susceptibility to severe COVID-19.
Sample genotype: GT (Heterozygous)
The G/T genotype indicates the presence of one copy of the T risk allele, which is a well-established risk factor for lung diseases [1]. This variant acts as a gain-of-function change, causing the MUC5B gene to produce excess mucin protein in the small airways [1]. Research indicates that this excess mucus can impair the lungs' ability to clear out debris, leading to chronic inflammation and scarring [2]. Clinical studies show a roughly 5-fold to 9-fold higher risk of developing idiopathic pulmonary fibrosis compared to the general population [2]. Interestingly, carrying this allele may offer a very slight protective effect against severe COVID-19 complications [3].
Moderately increased risk of pulmonary fibrosis; Slightly lower susceptibility to severe COVID-19.
Sample genotype: TT (Homozygous)
The T/T genotype represents the presence of two copies of the MUC5B promoter variant, which is the strongest known genetic risk factor for pulmonary fibrosis [1]. A dramatic increase in the production of mucin 5B, a gel-forming protein in the lungs, is driven by this genetic profile [1]. The resulting thick mucus accumulation is thought to cause ongoing microscopic injuries to the delicate air sacs, eventually leading to permanent scarring [2]. Clinical studies have found a 10-fold to over 20-fold higher risk of developing idiopathic pulmonary fibrosis for this profile [2]. While this risk is highly elevated, many people with this genotype never develop the disease, showing that environmental factors like smoking also play a major role [2].
Highly increased risk of pulmonary fibrosis; Substantially higher mucin 5B protein levels in the lungs.
Variants with shared genetic architecture
rs2076295 · DSP Gene · Chr 6 · Pulmonary Fibrosis Risk
rs11568819 · MMP7 Gene · Chr 11 · Lung Fibrosis and MMP7 Levels
rs7041 · GC Gene · Chr 4 · Vitamin D Levels
A variant in the promoter of MUC5B and idiopathic pulmonary fibrosis.
A common MUC5B promoter polymorphism and pulmonary fibrosis.
A first update on mapping the human genetic architecture of COVID-19.
Content updated August 2026.
ReadYourDNA provides educational interpretation of DNA data you already have. It is not diagnostic, not a substitute for professional medical advice, diagnosis, or treatment, and is not intended to diagnose, treat, cure, or prevent any disease. Talk to a clinician before acting on any result.
Raw DNA Data Reports for 23andMe & AncestryDNA · About ReadYourDNA · FAQ · Methodology & Science · Pricing · Support and complaints · Legal & Contact · Health Traits · Pharmacogenomics · Carrier Status · Variant Explorer · The Human Karyotype · Privacy Policy · Terms of Service · Accessibility · Consumer Health Data Privacy · Your Privacy Choices · Editorial Standards · Your Data, Checkable · Sample Report · ReadYourDNA and Promethease compared · What is inside a 23andMe raw data file · What is inside an AncestryDNA raw data file · What a chatbot can and cannot do with your raw DNA file · Where a raw DNA file can still be uploaded in 2026
Written, maintained and operated by Martin Pechhacker, sole proprietor, Vienna, Austria. Trade register GISA 40064420. support@readyourdna.com