ReviewGene2020
IFNL4: Notable variants and associated phenotypes
Review in Gene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Subtype-specific functions of basal IFNλs.Journal of virology · 2026Review
- Zika Virus: A Tale of Two Lineages.Pathogens (Basel, Switzerland) · 2025Review
- Interferon Lambda: The Next Frontier in Antiviral Therapy?Pharmaceuticals (Basel, Switzerland) · 2025Review
- An evolving understanding of multiple causal variants underlying genetic association signals.American journal of human genetics · 2025Review
- Structural studies of the IFNλ4 receptor complex using cryoEM enabled by protein engineering.Nature communications · 2025Article
- Frequencies of anInternational journal of molecular sciences · 2024Article
- Reduced IFNL1 and/or IFNL2, but not IFNL3 is associated with worse outcome in patients with COVID-19.Clinical and experimental immunology · 2024Article
- In search of a function for human type III interferons: insights from inherited and acquired deficits.Current opinion in immunology · 2024Review
- The adverse characteristics of hepatocellular carcinoma in the non-cirrhotic liver disproportionately disadvantage Black patients.Cancer medicine · 2024Article
- Variants ofGenes · 2023Article
- Pharmacogenomic Profile of Amazonian Amerindians.Journal of personalized medicine · 2022Article
- The role of IFNL4 in liver inflammation and progression of fibrosis.Genes and immunity · 2022Review
- Discordance in STING-Induced Activation and Cell Death Between Mouse and Human Dendritic Cell Populations.Frontiers in immunology · 2022Article
- Monocytes differentiated into macrophages and dendritic cells in the presence of human IFN-λ3 or IFN-λ4 show distinct phenotypes.Journal of leukocyte biology · 2021Article
- Review
- Stem cell-derived HCV infection systems illustrate the bright future of human hepatocyte research.Gut · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Interferon lambda proteins activate the JAK-STAT signalling pathway, resulting in upregulation of genes with antiviral effects. The interferon lambda family was initially thought to be redundant to the interferon alpha family, which signals through the same pathway, except for the more limited expression of the IFNLR1 receptor. However, recent studies show that interferon lambdas uniquely protect tissue barriers against a wide range of important viral infections. The interferon lambda 4 gene (IFNL4) was discovered in 2013. The IFNL4 protein is determined by the IFNL4-ΔG/TT (rs368234815) variant. The ancestral IFNL4-ΔG allele generates IFNL4, whereas IFNL4-TT causes pre-mature termination of the protein. Surprisingly, although interferons are generally antiviral proteins, the genotypes that generate the IFNL4 protein are strongly linked to impaired clearance of hepatitis C virus (HCV). IFNL4 genotype has also been linked to variation within the HCV genome, as well as risk of hepatic fibrosis, certain cancers and some infectious diseases. There has been very strong evolutionary selection against the ancestral IFNL4-ΔG allele, which is the major form in African populations, but the minor allele in Europeans and Asians. The reason for this selection and the biological mechanisms underlying observed phenotypic associations remain to be explained.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.