ReviewInternational journal of molecular sciences2019
Naturally Occurring Hepatitis B Virus Mutations Leading to Endoplasmic Reticulum Stress and Their Contribution to the Progression of Hepatocellular Carcinoma.
Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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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.
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Who cites it
55 citing papers in PubMed, 104 citations in OpenAlex.
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- The impact of single-nucleotide variants of hepatitis B virus and antiviral on liver cancer in gray zone patients.Journal of biomedical science · 2025Article
- Comprehensive evaluation of NAT+/HBsAg- blood donors: confirmation strategies, serial testing outcomes, and S gene mutations associated with occult HBV infection.BMC infectious diseases · 2025Article
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- Increased ROS levels activate AMPK-ULK1-mediated mitophagy to promote pseudorabies virus replication.Veterinary research · 2025Article
- Surface Gene Mutations of Hepatitis B Virus and Related Pathogenic Mechanisms: A Narrative Review.Viruses · 2025Review
- Detectable Hepatitis B Virus (HBV) PreS Deletion Mutants at Baseline Predicted Delayed Immune Reconstitution and Increased Inflammation in People With Human Immunodeficiency Virus and HBV Coinfection Undergoing Long-term Antiretroviral Therapy.Open forum infectious diseases · 2025Article
- The spatiotemporal heterogeneity of reactive oxygen species in the malignant transformation of viral hepatitis to hepatocellular carcinoma: a new insight.Cellular & molecular biology letters · 2025Review
- PreS1 deletions in genotype C HBV leads to severe hepatic inflammation and hepatocarcinogenesis via the IRE1-JNK axis.JHEP reports : innovation in hepatology · 2025Article
- The Malignant Transformation of Viral Hepatitis to Hepatocellular Carcinoma: Mechanisms and Interventions.MedComm · 2025Review
- Current status and new directions for hepatocellular carcinoma diagnosis.Liver research (Beijing, China) · 2024Review
- Hepatitis B Virus X Protein Induces Reactive Oxygen Species Generation via Activation of p53 in Human Hepatoma Cells.Biomolecules · 2024Article
- Review
- The impact of integrated hepatitis B virus DNA on oncogenesis and antiviral therapy.Biomarker research · 2024Review
- Occult Hepatitis B Virus Infection in Hepatic Diseases and Its Significance for the WHO's Elimination Plan of Viral Hepatitis.Pathogens (Basel, Switzerland) · 2024Review
- Article
- Reactive Oxygen Species Induction by Hepatitis B Virus: Implications for Viral Replication in p53-Positive Human Hepatoma Cells.International journal of molecular sciences · 2024Article
- miRNA‑mRNA network contributes to HBV‑related hepatocellular carcinoma via immune infiltration induced by GRB2.Biomedical reports · 2024Article
- Hepatitis B surface antigen expression impairs endoplasmic reticulum stress-related autophagic flux by decreasing LAMP2.JHEP reports : innovation in hepatology · 2024Article
- Hepatitis B Surface Antigen Isoforms: Their Clinical Implications, Utilisation in Diagnosis, Prevention and New Antiviral Strategies.Pathogens (Basel, Switzerland) · 2024Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Hepatitis B virus (HBV) infection is a global health problem that causes a wide range of pathological outcomes, including cirrhosis and hepatocellular carcinoma (HCC). Endoplasmic reticulum (ER) stress induction by HBV infection has been implicated in liver carcinogenesis and disease progression with chronic inflammation via enhanced inflammation, oxidative stress-mediated DNA damage, and hepatocyte proliferation. In the natural course of HBV infection, the accumulation of naturally occurring mutations in the HBV genome can generate several mutant types of HBV-encoded proteins, including three different proteins in the S ORF (SHBs, MHBs, and LHBs) and HBcAg in the C ORF, which could contribute to enhanced ER stress in infected hepatocytes mainly via increased ER accumulation of mutant proteins. However, it seems that there may be distinct capacity and pathway in ER stress-induction and distinct resulting clinical outcomes between HBV variants. In addition, the role of HBxAg mutations in ER stress remains unknown. However, it has been reported that HBxAg itself could exert ER stress in infected cells, resulting in HCC generation in chronic HBV patients. To date, review papers regarding ER stress-mediated HBV mutation have been limited into a specific mutation type: preS2 deletion. So, in this review, we will discuss details about various mutation types in all four regions of the HBV genome (preS1, preS2, S, and C) related to ER stress and their distinct ER stress mechanisms and clinical outcomes in terms of mutation types.
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