ArticleMolecular therapy : the journal of the American Society of Gene Therapy2021
ADAR1 Stimulation by IFN-α Downregulates the Expression of MAVS via RNA Editing to Regulate the Anti-HBV Response.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 26 citations in OpenAlex.
- Aloe emodin isolated frommSphere · 2026Article
- The mitochondrial GTPase ERAL1 inhibits HBV replication by triggering the MAVS signaling cascade.Journal of translational medicine · 2026Article
- Innate immune recognition and evasion strategies of hepatitis B virus: from DNA to RNA and viral proteins.Frontiers in immunology · 2026Review
- ADAR1: a central regulator of dsRNA sensing in host-virus interactions.Frontiers in immunology · 2026Review
- Old dogs-new tricks: multifaceted functions of MAVS beyond antivirus activity in human health and diseases.Cell & bioscience · 2025Review
- ADARs: pleiotropy in function, versatility in application.Nucleic acids research · 2025Review
- HBc: the multifunctional architect of HBV replication, immune evasion, and therapeutic innovation.Frontiers in immunology · 2025Review
- The role of ADAR1 in human pathophysiology.Frontiers in cell and developmental biology · 2025Review
- Current status and challenges of therapeutic targets, novel drugs and delivery systems for hepatitis B: how far to our goal?Frontiers in cellular and infection microbiology · 2025Review
- The Application of Base-Editing Technology to Investigate Virus-Host Interactions and Antiviral Therapeutic Strategies.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Inflammatory factors collaboratively linkFrontiers in immunology · 2025Review
- RNA editing in host lncRNAs as potential modulator in SARS-CoV-2 variants-host immune response dynamics.iScience · 2024Article
- Dopamine Inhibits the Expression of Hepatitis B Virus Surface and e Antigens by Activating the JAK/STAT Pathway and Upregulating Interferon-stimulated Gene 15 Expression.Journal of clinical and translational hepatology · 2024Article
- An HBV susceptibility variant of KNG1 modulates the therapeutic effects of interferons α and λ1 in HBV infection by promoting MAVS lysosomal degradation.EBioMedicine · 2023Article
- Article
- [Interferon-related gene array in predicting the efficacy of interferon therapy in chronic hepatitis B].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2023Article
- Quantification of AMPA receptor subunits and RNA editing-related proteins in the J20 mouse model of Alzheimer's disease by capillary western blotting.Frontiers in molecular neuroscience · 2023Article
- The regulation of antiviral innate immunity through non-mFrontiers in immunology · 2023Review
- lncRNA XLOC013218 promotes cell proliferation and TMZ resistance by targeting the PIK3R2-mediated PI3K/AKT pathway in glioma.Cancer science · 2022Article
- Interferon Alpha Induces Cellular Autophagy and Modulates Hepatitis B Virus Replication.Frontiers in cellular and infection microbiology · 2022Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The partial response of chronic hepatitis B virus (CHB) patients to interferon-α (IFN-α) therapy remains elusive, which requires a better understanding of the involved molecular mechanism. In our study, bioinformatics analysis was applied to relate IFN-α regulated candidate genes and RNA editing sites by RNA sequencing. Mitochondrial antiviral signaling protein (MAVS) antiviral effect was confirmed in HepG2.2.15 cells and in two mouse models. The associations between polymorphisms in MAVS gene and response to IFN-α therapy were confirmed in CHB patients. We found that IFN-α downregulates MAVS via RNA editing that was mediated by adenosine deaminase acting on RNA (ADAR1). ADAR1 inhibited MAVS expression via a human antigen R (HuR)-mediated post-transcriptional regulation. MAVS exerted an antiviral activity and reduced the level of hepatitis B virus (HBV) markers in vitro and in vivo. IFN-α antiviral effects were significantly enhanced by MAVS co-transfection. Hepatitis B core protein (HBc) interacted with SP1 to inhibit the promoter activity of MAVS that regulates its expression. CHB patients with a rs3746662A allele had higher MAVS expression and thus were more responsive to IFN-α treatment. In this work, we demonstrated that the decrease of MAVS expression is mediated by the IFN-α-ADAR1 axis. This study also highlighted the potential for the clinical application of MAVS in combination with IFN-α for the treatment of HBV infection.
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