ArticleJournal of virology2017
Matrix Metalloproteinase 9 Facilitates Hepatitis B Virus Replication through Binding with Type I Interferon (IFN) Receptor 1 To Repress IFN/JAK/STAT Signaling.
Article in Journal of virology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 79 citations in OpenAlex.
- Failed immune responses across multiple pathologies share pan-tumor and circulating lymphocytic targets.The Journal of clinical investigation · 2019Trial
- Hepatocellular carcinoma metastasis-immune microenvironment crosstalk: emerging mechanisms and immunotherapy.Cellular & molecular biology letters · 2026Review
- MMP-9 regulates disulphide isomerase activity of TGM2 to enhance fusion glycoprotein-mediated syncytium formation of respiratory syncytial virus.Protein & cell · 2026Article
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- Innate immune recognition in hepatitis B virus infection.Virulence · 2025Review
- PIM1 Attenuates Innate Immunity to Foster Coronavirus Replication through Ubiquitin Ligase β-TrCP-Mediated IFNAR1 Degradation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- MicroRNA-140-5p and cystatin-C expression in patients with vascular cognitive impairment and its clinical value.Biomarkers in medicine · 2025Article
- The African swine fever virus p22 inhibits the JAK-STAT signaling pathway by promoting the TAX1BP1-mediated degradation of the type I interferon receptor.PLoS pathogens · 2025Article
- A reliable prognostic model for hepatocellular carcinoma using neutrophil extracellular traps and immune related genes.Scientific reports · 2025Article
- Epigenetic regulation and its therapeutic potential in hepatitis B virus covalently closed circular DNA.Genes & diseases · 2025Review
- Host proteases: key regulators in viral infection and therapeutic targeting.Frontiers in immunology · 2025Review
- Chinese medicine in the treatment of chronic hepatitis B: The mechanisms of signal pathway regulation.Heliyon · 2024Review
- In Memory of the Virologist Jianguo Wu, 1957-2022.Viruses · 2023Article
- Transcriptome wide functional analysis of HBx expressing human hepatocytes stimulated with endothelial cell cross-talk.Genomics · 2023Article
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- Exploring the mechanism of JiGuCao capsule formula on treating hepatitis B virus infection via network pharmacology analysis andFrontiers in pharmacology · 2023Article
- Article
- Review
- Hepatitis B virus promotes hepatocellular carcinoma development by activating GP73 to repress the innate immune response.Infectious agents and cancer · 2022Article
- IFITM3 Interacts with the HBV/HDV Receptor NTCP and Modulates Virus Entry and Infection.Viruses · 2022Article
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis B virus (HBV) infection may cause acute hepatitis B, chronic hepatitis B (CHB), liver cirrhosis, and hepatocellular carcinoma (HCC). However, the mechanisms by which HBV evades host immunity and maintains chronic infection are largely unknown. Here, we revealed that matrix metalloproteinase 9 (MMP-9) is activated in peripheral blood mononuclear cells (PBMCs) of HBV-infected patients, and HBV stimulates MMP-9 expression in macrophages and PBMCs isolated from healthy individuals. MMP-9 plays important roles in the breakdown of the extracellular matrix and in the facilitation of tumor progression, invasion, metastasis, and angiogenesis. MMP-9 also regulates respiratory syncytial virus (RSV) replication, but the mechanism underlying such regulation is unknown. We further demonstrated that MMP-9 facilitates HBV replication by repressing the interferon (IFN)/Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway, IFN action, STAT1/2 phosphorylation, and IFN-stimulated gene (ISG) expression. Moreover, MMP-9 binds to type I IFN receptor 1 (IFNAR1) and facilitates IFNAR1 phosphorylation, ubiquitination, subcellular distribution, and degradation to interfere with the binding of IFANR1 to IFN-α. Thus, we identified a novel positive-feedback regulation loop between HBV replication and MMP-9 production. On one hand, HBV activates MMP-9 in infected patients and leukocytes. On the other hand, MMP-9 facilitates HBV replication through repressing IFN/JAK/STAT signaling, IFNAR1 function, and IFN-α action. Therefore, HBV may take the advantage of MMP-9 function to establish or maintain chronic infection.
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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.