ArticleScientific reports2017
Hepatitis B Virus e Antigen Activates the Suppressor of Cytokine Signaling 2 to Repress Interferon Action.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 34 citations in OpenAlex.
- Article
- The clinical significance and optimization strategies of HBeAg seroclearance in chronic hepatitis B treatment.Frontiers in cellular and infection microbiology · 2026Review
- The interferon-inducible MxB large GTPase attenuates hepatitis B virus replication by activating the RIG-I innate immunity signaling pathway.Scientific reports · 2025Article
- In Memory of the Virologist Jianguo Wu, 1957-2022.Viruses · 2023Article
- The Complex Role of HBeAg and Its Precursors in the Pathway to Hepatocellular Carcinoma.Viruses · 2023Review
- Treatment of Liver Fibrosis after Hepatitis B with TCM Combined with NAs Evaluated by Noninvasive Diagnostic Methods: A Retrospective Study.Evidence-based complementary and alternative medicine : eCAM · 2023Article
- Oncolytic Vaccinia Virus HarboringMarine drugs · 2022Article
- Regulation of Pattern-Recognition Receptor Signaling by HBX During Hepatitis B Virus Infection.Frontiers in immunology · 2022Review
- Hepatitis B virus e antigen and viral persistence.Current opinion in virology · 2021Review
- Specific determination of hepatitis B e antigen by antibodies targeting precore unique epitope facilitates clinical diagnosis and drug evaluation against hepatitis B virus infection.Emerging microbes & infections · 2021Article
- MafF Is an Antiviral Host Factor That Suppresses Transcription from Hepatitis B Virus Core Promoter.Journal of virology · 2021Article
- Review of Lambda Interferons in Hepatitis B Virus Infection: Outcomes and Therapeutic Strategies.Viruses · 2021Review
- Antiviral mechanism of preclinical antimalarial compounds possessing multiple antiviral activities.FASEB bioAdvances · 2021Article
- Intracellular interferon signalling pathways as potential regulators of covalently closed circular DNA in the treatment of chronic hepatitis B.World journal of gastroenterology · 2021Review
- Transcriptome Classification Reveals Molecular Subgroups in Patients with Hepatitis B Virus.Computational and mathematical methods in medicine · 2021Article
- Factors associated with disease progression and viral replication in patients with chronic hepatitis B virus infection.Experimental and therapeutic medicine · 2019Article
- MicroRNA-196a/-196b regulate the progression of hepatocellular carcinoma through modulating the JAK/STAT pathway via targeting SOCS2.Cell death & disease · 2019Article
- Article
- Article
- Structures of Hepatitis B Virus Core- and e-Antigen Immune Complexes Suggest Multi-point Inhibition.Structure (London, England : 1993) · 2018Article
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis B virus (HBV) infection causes acute hepatitis B (AHB), chronic hepatitis B (CHB), liver cirrhosis (LC), and eventually hepatocellular carcinoma (HCC). The presence of hepatitis B e antigen (HBeAg) in the serum generally indicates ongoing viral replication and disease progression. However, the mechanism by which HBeAg regulates HBV infection remains unclear. Interferons (IFNs) are pleiotropic cytokines that participate in host innate immunity. After binding to receptors, IFNs activate the JAK/STAT pathway to stimulate expression of IFN-stimulated genes (ISGs), leading to induction of antiviral responses. Here, we revealed that HBeAg represses IFN/JAK/STAT signaling to facilitate HBV replication. Initially, HBeAg stimulates the expression of suppressor of cytokine signaling 2 (SOCS2). Subsequently, SOCS2 impairs IFN/JAK/STAT signaling through reducing the stability of tyrosine kinase 2 (TYK2), downregulating the expression of type I and III IFN receptors, attenuating the phosphorylation and nucleus translocation of STAT1. Finally, SOCS2 inhibits the expression of ISGs, which leads to the repression of IFN action and facilitation of viral replication. These results demonstrate an important role of HBeAg in the regulation of IFN action, and provide a possible molecular mechanism by which HBV resists the IFN therapy and maintains persistent infection.
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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.