Related Experiment Video

Updated: Jun 2, 2026

Analysis of HBV-Specific CD4 T-cell Responses and Identification of HLA-DR-Restricted CD4 T-Cell Epitopes Based on a Peptide Matrix
10:37

Analysis of HBV-Specific CD4 T-cell Responses and Identification of HLA-DR-Restricted CD4 T-Cell Epitopes Based on a Peptide Matrix

Published on: October 20, 2021

A336C/A336T/T337C variations in HBV core gene and spontaneous hepatitis B e antigen loss in chronic hepatitis B

Wen Fan1, Lu Huang, Zhiming Zhou

  • 1Laboratory Department, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China 430022.

Virology Journal
|May 17, 2011
PubMed

Insights

Hepatitis B virus (HBV) core gene variations, specifically A336C/A336T/T337C, are linked to spontaneous HBeAg loss in chronic hepatitis B patients. These genetic variations are identified as independent factors associated with this significant clinical outcome.

Area of Science:

  • Virology
  • Hepatology
  • Genetics

Background:

  • Hepatitis B virus (HBV) core gene variations A336C/A336T/T337C correlate with reduced HBV DNA levels and replication.
  • Spontaneous loss of Hepatitis B e-antigen (HBeAg) is typically associated with a significant decrease in serum HBV DNA levels.

Purpose of the Study:

  • To investigate the association between A336C/A336T/T337C variations in the HBV core gene and spontaneous HBeAg loss in chronic hepatitis B patients.

Main Methods:

  • A modified PCR-RFLP assay was used to detect A336C/A336T/T337C variations.
  • ELISA determined serum HBeAg levels, while Taqman-PCR identified G1896A variation and HBV genotype.
  • Statistical analyses, including Chi-square and binary logistic regression, were employed.

Main Results:

  • A336C/A336T/T337C variations were found in 24.1% of chronic hepatitis B patients.
  • These variants were more frequent in patients with the A1896 variation and were associated with a lower HBeAg-positive percentage.
  • Genotype B, C336/T336/C337 variants, and A1896 variants were identified as independent factors for spontaneous HBeAg loss.

Conclusions:

  • A336C/A336T/T337C represent naturally occurring polymorphisms in the HBV core gene.
  • The presence of C336/T336/C337 variants is a novel, independent predictor of spontaneous HBeAg loss in chronic hepatitis B.
Abstract

More Related Videos

Detection of Low Copy Number Integrated Viral DNA Formed by In Vitro Hepatitis B Infection11:14

Detection of Low Copy Number Integrated Viral DNA Formed by In Vitro Hepatitis B Infection

Published on: November 7, 2018

Stem Cell-Derived Viral Ag-Specific T Lymphocytes Suppress HBV Replication in Mice07:25

Stem Cell-Derived Viral Ag-Specific T Lymphocytes Suppress HBV Replication in Mice

Published on: September 25, 2019

Related Concept Videos

Hepatitis01:25

Hepatitis

Hepatitis is an inflammatory condition of the liver most commonly caused by hepatotropic viruses (A–E), though non-infectious causes such as alcohol and drugs also exist.Hepatitis AHepatitis A virus (HAV) is a non-enveloped RNA virus of the Picornaviridae family. It is primarily transmitted via the fecal-oral route, typically through ingestion of contaminated food or water. After ingestion, HAV enters the bloodstream through the oropharynx or intestinal epithelium and reaches the liver. The...
Viral Hepatitis I: Introduction01:28

Viral Hepatitis I: Introduction

Viral hepatitis is an inflammatory condition of the liver caused by infection with hepatotropic viruses, most commonly hepatitis A, B, C, D, and E. Despite variations in structure and transmission, all viruses mentioned infect hepatocytes and provoke immune responses that can hinder liver function. Additionally, some non-hepatotropic viruses can also lead to hepatic inflammation.Hepatitis A VirusHepatitis A virus (HAV) is transmitted through the fecal–oral route, typically by ingestion of food...
Viral Mutations00:36

Viral Mutations

A mutation is a change in the sequence of bases of DNA or RNA in a genome. Some mutations occur during replication of the genome due to errors made by the polymerase enzymes that replicate DNA or RNA. Unlike DNA polymerase, RNA polymerase is prone to errors because it is not capable of “proofreading” its work. Viruses with RNA-based genomes, like HIV, therefore accrue mutations faster than viruses with DNA-based genomes. Because mutation and recombination provide the raw material for adaptive...
Exon Recombination02:32

Exon Recombination

The evolution of new genes is critical for speciation. Exon recombination, also known as exon shuffling or domain shuffling, is an important means of new gene formation. It is observed across vertebrates, invertebrates, and in some plants such as potatoes and sunflowers. During exon recombination, exons from the same or different genes recombine and produce new exon-intron combinations, which might evolve into new genes. 
Exon shuffling follows “splice frame rules.” Each exon has three reading...
Cirrhosis II: Pathophysiology01:24

Cirrhosis II: Pathophysiology

Cirrhosis is a progressive chronic liver injury caused by prolonged inflammation, excessive fibrotic remodeling, and impaired regeneration. Over time, repeated hepatic insults disrupt the liver’s architecture and function, leading to reduced blood flow, impaired bile drainage, and diminished metabolic capacity.Pathophysiology of cirrhosisCirrhosis arises from three main responses to chronic liver damage: inflammation, immune activation, and hepatocyte death. These processes lead to structural...
Diseases of the Liver and Gallbladder01:26

Diseases of the Liver and Gallbladder

Liver and gallbladder diseases are a significant health concern, with prominent conditions including cirrhosis, hepatitis, non-alcoholic fatty liver disease (NAFLD), and gallstones. Jaundice is a common manifestation of liver and biliary disease.
Cirrhosis is characterized by the scarring of hepatic lobules in the liver, which are replaced by fibrous tissue, affecting the liver's normal functioning. NAFLD, on the other hand, is caused by an excessive build-up of fat in the liver, not related to...