HBV Mutation Detail Information

Virus Mutation HBV Mutation A181T


Basic Characteristics of Mutations
Mutation Site A181T
Mutation Site Sentence Wild-Type and rtA181T/sW172* Mutant Strains of Hepatitis B Virus Drive Hepatocarcinogenesis via Distinct GRP78-Mediated ER Stress Pathways.
Mutation Level Amino acid level
Mutation Type Nonsynonymous substitution
Gene/Protein/Region RT
Standardized Encoding Gene P  
Genotype/Subtype -
Viral Reference -
Functional Impact and Mechanisms
Disease Hepatitis B Virus Infection    
Immune -
Target Gene -
Clinical and Epidemiological Correlations
Clinical Information -
Treatment -
Location -
Literature Information
PMID 39749680
Title Wild-Type and rtA181T/sW172* Mutant Strains of Hepatitis B Virus Drive Hepatocarcinogenesis via Distinct GRP78-Mediated ER Stress Pathways
Author Liu M,Yuan M,Ma Y,Wang J,Cheng X,Shi Y,Shang J,He M,Bai L,Du L,Tang H
Journal Journal of medical virology
Journal Info 2025 Jan;97(1):e70151
Abstract Glucose-regulated protein 78 kDa (GRP78), a key marker of endoplasmic reticulum stress (ERS), is upregulated in hepatocellular carcinoma (HCC) tissues, but its role in hepatitis B virus (HBV)-induced tumorigenesis remains unclear. This study aimed to investigate the contribution of GRP78 to HBV-associated tumor development and explore the ERS pathways involved. The results showed that increased GRP78 expression in patients with HBV-related HCC was associated with a poor prognosis within the first 2 years following diagnosis. Furthermore, using wild-type HBV strain and the oncogenic HBV rtA181T/sW172* mutant, this study demonstrated that the HBV-induced GRP78 expression correlated with elevated reactive oxygen species (ROS) levels. Moreover, GRP78 expression enhanced hepatocyte proliferation and resistance to apoptosis. In wild-type HBV-infected hepatocytes, GRP78 suppressed apoptosis by inhibiting the PERK/p38 pathway. In contrast, the HBV rtA181T/sW172* mutation led to increased GRP78 expression and inhibition of cell apoptosis through activation of the IRE-1alpha/XBP1/BCL-2 pathway. In conclusion, GRP78 plays a pivotal role in HBV-induced hepatocarcinogenesis by modulating distinct ERS pathways. Targeting these pathways may aid in the therapeutic management of HBV-associated hepatocarcinogenesis.
Sequence Data -
Mutation Information
Note
Basic Characteristics of Mutations
  • Mutation Site: The specific location in a gene or protein sequence where a change occurs.
  • Mutation Level: The level at which a mutation occurs, including the nucleotide or amino acid level.
  • Mutation Type: The nature of the mutation, such as missense mutation, nonsense mutation, synonymous mutation, etc.
  • Gene/Protein/Region: Refers to the specific region of the virus where the mutation occurs. Including viral genes, viral proteins, or a specific viral genome region. If the article does not specifically indicate the relationship between the mutation and its correspondence, the main
  • Gene/Protein/Region studied in the article is marked.
  • Genotype/Subtype: Refers to the viral genotype or subtype where the mutation occurs. If the article does not specifically indicate the relationship between the mutation and its correspondence, the main Genotype/Subtype studied in the article is marked.
  • Viral Reference: Refers to the standard virus strain used to compare and analyze viral sequences.
Functional Impact and Mechanisms
  • Disease: An abnormal physiological state with specific symptoms and signs caused by viral infection.
  • Immune: The article focuses on the study of mutations and immune.
  • Target Gene: Host genes that viral mutations may affect.
Clinical and Epidemiological Correlations
  • Clinical Information: The study is a clinical or epidemiological study and provides basic information about the population.
  • Treatment: The study mentioned a certain treatment method, such as drug resistance caused by mutations. If the study does not specifically indicate the relationship between mutations and their correspondence treatment, the main treatment studied in the article is marked.
  • Location: The source of the research data.
Literature Information
  • Sequence Data: The study provides the data accession number.