ArticleScientific reports2016
STAT1 is essential for the inhibition of hepatitis C virus replication by interferon-λ but not by interferon-α.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- The potential of IFN-λ, IL-32γ, IL-6, and IL-22 as safeguards against human viruses: a systematic review and a meta-analysis.Frontiers in immunology · 2024Pooled it
- A scalable proteogenomic framework for dissecting phospho-signaling pathways in primary immune cells.bioRxiv : the preprint server for biology · 2025Article
- Dose-Dependent Porcine Deltacoronavirus Infection Reveals Linkage Between Infectious Dose and Immune Response.Animals : an open access journal from MDPI · 2025Article
- CRISPR/Cas9 as a New Antiviral Strategy for Treating Hepatitis Viral Infections.International journal of molecular sciences · 2023Review
- ISGF3 and STAT2/IRF9 Control Basal and IFN-Induced Transcription through Genome-Wide Binding of Phosphorylated and Unphosphorylated Complexes to Common ISRE-Containing ISGs.International journal of molecular sciences · 2023Article
- CRISPR-Cas system to discover host-virus interactions in Flaviviridae.Virology journal · 2023Review
- A Synopsis of Hepatitis C Virus Treatments and Future Perspectives.Current issues in molecular biology · 2023Review
- Article
- Article
- Interferon regulatory factor 1 (IRF1) inhibits lung endothelial regeneration following inflammation-induced acute lung injury.Clinical science (London, England : 1979) · 2023Article
- IFN-Inducible SerpinA5 Triggers Antiviral Immunity by Regulating STAT1 Phosphorylation and Nuclear Translocation.International journal of molecular sciences · 2023Article
- STAT1 and Its Crucial Role in the Control of Viral Infections.International journal of molecular sciences · 2022Review
- Antiviral strategies targeting host factors and mechanisms obliging +ssRNA viral pathogens.Bioorganic & medicinal chemistry · 2021Review
- Novel interferon-sensitive genes unveiled by correlation-driven gene selection and systems biology.Scientific reports · 2021Article
- Review
- Signatures of immune dysfunction in HIV and HCV infection share features with chronic inflammation in aging and persist after viral reduction or elimination.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- HLA Class I Upregulation and Antiviral Immune Responses in Graves Disease.The Journal of clinical endocrinology and metabolism · 2021Article
- Evolutionary Pattern of Interferon Alpha Genes in Bovidae and Genetic Diversity of IFNAA in the Bovine Genome.Frontiers in immunology · 2020Article
- DMPK is a New Candidate Mediator of Tumor Suppressor p53-Dependent Cell Death.Molecules (Basel, Switzerland) · 2019Article
- HCV and flaviviruses hijack cellular mechanisms for nuclear STAT2 degradation: Up-regulation of PDLIM2 suppresses the innate immune response.PLoS pathogens · 2019Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interferon-α (IFN-α) and IFN-λ are structurally distinct cytokines that bind to different receptors, but induce expression of similar sets of genes through Janus kinase (JAK)-signal transducers and activators of transcription (STAT) pathways. The difference between IFN-α and IFN-λ signaling remains poorly understood. Here, using the CRISPR/Cas9 system, we examine the role of STAT1 and STAT2 in the inhibition of hepatitis C virus (HCV) replication by IFN-α and IFN-λ. Treatment with IFN-α increases expression of IFN-stimulated genes (ISGs) such as double-stranded RNA-activated protein kinase (PKR) and decreases viral RNA and protein levels in HCV-infected Huh-7.5 human hepatoma cells. These responses are only partially attenuated by knockout of STAT1 but are abolished by knockout of STAT2. In contrast, the inhibition of HCV replication by IFN-λ is abolished by knockout of STAT1 or STAT2. Microarray analysis reveals that IFN-α but not IFN-λ can induce expression of the majority of ISGs in STAT1 knockout cells. These findings suggest that IFN-α can inhibit HCV replication through a STAT2-dependent but STAT1-independent pathway, whereas IFN-λ induces ISG expression and inhibits HCV replication exclusively through a STAT1- and STAT2-dependent pathway.
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Registered trials
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