ReviewVirology journal2024
Mechanisms underlying the compromised clinical efficacy of interferon in clearing HBV.
Review in Virology journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed.
- [Advancement in the role of exosomes for hepatitis B virus infection diagnosis and treatment: mechanisms and clinical applications].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026Review
- Liver Macrophages in the Pathogenesis of Viral Hepatitis.Current issues in molecular biology · 2026Review
- Precise delivery of medical gases by engineered nanomedicine for enhanced liver fibrosis therapy.Materials today. Bio · 2026Review
- [Expert recommendations on the management of adverse reactions in pegylated interferon alpha therapy for chronic hepatitis B].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026Article
- Predictive value and mechanism of LINC00665 for liver dysfunction in pregnant women with hepatitis B during early pregnancy.Virology journal · 2026Article
- Repurposing Product Nkabinde for Hepatitis B Virus Therapy: A Network Pharmacology and Molecular Docking Investigation.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Sustained HBsAg clearance induced by pegylated interferon α-2b in HBeAg-negative patients with low baseline HBsAg.Frontiers in cellular and infection microbiology · 2026Article
- PYHIN proteins: guardians or contributors to hepatitis B virus pathogenesis?Frontiers in immunology · 2026Review
- Interferon therapy for chronic hepatitis B in children: an immunological perspective.Frontiers in immunology · 2026Review
- Review
- Do the therapeutic vaccines hold hope for the treatment of hepatitis B?Hepatology international · 2025Review
- Hepatitis B functional cure: Current and future perspective.World journal of hepatology · 2025Review
- Exosome in HBV infection: current concepts and future perspectives.Frontiers in cellular and infection microbiology · 2025Review
- Genetic association betweenFrontiers in genetics · 2025Article
- Bioinformatics and system biology approach to discover the common pathogenetic processes between COVID-19 and chronic hepatitis B.PloS one · 2025Article
- Virus-host interaction mechanisms in interferon therapy for hepatitis B virus infection: recent advances.Frontiers in immunology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Hepatitis B virus (HBV) is a hepatotropic DNA virus that can cause acute or chronic hepatitis, representing a significant global health concern. By 2019, approximately 296 million individuals were chronically infected with HBV, with 1.5 million new cases annually and 820,000 deaths due to HBV-related cirrhosis and liver cancer. Current treatments for chronic hepatitis B include nucleotide analogs (NAs) and interferons (IFNs), particularly IFN-α. NAs, such as entecavir and tenofovir, inhibit viral reverse transcription, while IFN-α exerts antiviral effects by directly suppressing viral replication, modulating viral genome epigenetics, degrading cccDNA, and activating immune responses. Despite its potential, IFN-α shows limited clinical efficacy, partly due to HBV's interference with the IFN signaling pathway. HBV encodes proteins like HBc, Pol, HBsAg, and HBx that disrupt IFN-α function. For example, HBV Pol inhibits STAT1 phosphorylation, HBsAg suppresses STAT3 phosphorylation, and HBx interferes with IFN-α efficacy through multiple mechanisms. Additionally, HBV downregulates key genes in the IFN signaling pathway, further diminishing IFN-α's antiviral effects. Understanding these interactions is crucial for improving IFN-α-based therapies. Future research may focus on overcoming HBV resistance by targeting viral proteins or optimizing IFN-α delivery. In summary, HBV's ability to resist IFN-α limits its therapeutic effectiveness, highlighting the need for new strategies to enhance treatment outcomes.
Indexed as
Identifiers
What Socratic 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 Socratic graph.