ReviewBiomedicines2022
Hepatitis B x (HBx) as a Component of a Functional Cure for Chronic Hepatitis B.
Review in Biomedicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 18 citations in OpenAlex.
- Hepatitis B core-related antigen as a multifaceted biomarker in chronic hepatitis B: implications for immune activity and hepatocellular carcinoma prediction.The Korean journal of internal medicine · 2026Article
- An overview of hepatitis B virus in gastric carcinogenesis: from clinical association to molecular mechanisms.Infectious agents and cancer · 2025Review
- HBV DNA integration gene CCDC91 is oncogenic and a potential therapeutic target for hepatocellular carcinoma.Communications biology · 2025Article
- HBx Drives Liver Cancer Stem Cell Generation Through Stimulating Glucose Metabolic Reprogramming.Journal of cellular and molecular medicine · 2025Article
- The Intrinsically Disordered Region of HBx and Virus-Host Interactions: Uncovering New Therapeutic Approaches for HBV and Cancer.International journal of molecular sciences · 2025Review
- HBV-Induced Carcinogenesis: Mechanisms, Correlation With Viral Suppression, and Implications for Treatment.Liver international : official journal of the International Association for the Study of the Liver · 2025Review
- Postoperative hepatitis B virus reactivation and its impact on survival in HBV-related hepatocellular carcinoma patients undergoing conversion therapy with interventional therapy combined with tyrosine kinase inhibitors and immune checkpoint inhibitors.Frontiers in cellular and infection microbiology · 2025Article
- HBx induces chemoresistance in diffuse large B cell lymphoma by inhibiting intrinsic apoptosis via the NF-κB/XIAP pathway.Molecular therapy. Nucleic acids · 2024Article
- New thiourea derivatives that target the episomal silencing SMC5 protein to inhibit HBx-dependent viral DNA replication and gene transcription.Virusdisease · 2024Article
- Overview of the immunological mechanisms in hepatitis B virus reactivation: Implications for disease progression and management strategies.World journal of gastroenterology · 2024Review
- The Epidemiology, Transmission, Genotypes, Replication, Serologic and Nucleic Acid Testing, Immunotolerance, and Reactivation of Hepatitis B Virus.Gastro hep advances · 2024Review
- Autophagy modulates physiologic and adaptive response in the liver.Liver research (Beijing, China) · 2023Review
- Relevance of HBx for Hepatitis B Virus-Associated Pathogenesis.International journal of molecular sciences · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Patients who are carriers of the hepatitis B virus (HBV) are at high risk of chronic liver disease (CLD) which proceeds from hepatitis, to fibrosis, cirrhosis and to hepatocellular carcinoma (HCC). The hepatitis B-encoded X antigen, HBx, promotes virus gene expression and replication, protects infected hepatocytes from immunological destruction, and promotes the development of CLD and HCC. For virus replication, HBx regulates covalently closed circular (ccc) HBV DNA transcription, while for CLD, HBx triggers cellular oxidative stress, in part, by triggering mitochondrial damage that stimulates innate immunity. Constitutive activation of NF-κB by HBx transcriptionally activates pro-inflammatory genes, resulting in hepatocellular destruction, regeneration, and increased integration of the HBx gene into the host genome. NF-κB is also hepatoprotective, which sustains the survival of infected cells. Multiple therapeutic approaches include direct-acting anti-viral compounds and immune-stimulating drugs, but functional cures were not achieved, in part, because none were yet devised to target HBx. In addition, many patients with cirrhosis or HCC have little or no virus replication, but continue to express HBx from integrated templates, suggesting that HBx contributes to the pathogenesis of CLD. Blocking HBx activity will, therefore, impact multiple aspects of the host-virus relationship that are relevant to achieving a functional cure.
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.