Related Experiment Video

Updated: Apr 16, 2026

Detection of Low Copy Number Integrated Viral DNA Formed by In Vitro Hepatitis B Infection
11:14

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

Published on: November 7, 2018

19.0K

Mutations of Basal core promoter and precore regions in hepatitis B virus genotypes B and C

Yong Huang1, Haijun Deng2, Zhi Peng3

  • 1The Key Laboratory of Molecular Biology of Infectious Diseases Designated by the Chinese Ministry of Education, Chongqing Medical University, Chongqing, China ; Department of Clinical Laboratory, Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.

Hepatitis Monthly
|March 6, 2015
PubMed

Insights

Hepatitis B virus (HBV) basal core promoter (BCP) and precore mutations differ significantly between genotypes B and C in children, with unique combined mutations found in genotype C children. These mutations are linked to higher viral loads and younger age.

Area of Science:

  • Hepatology and Virology
  • Molecular Biology
  • Pediatric Infectious Diseases

Background:

  • Mutations in the basal core promoter (BCP) and precore regions of the hepatitis B virus (HBV) are linked to disease progression and treatment response in chronic HBV infection.
  • Previous studies have focused on BCP and precore mutation analysis in adults across different HBV genotypes.
  • Such analyses are notably underrepresented in chronically infected pediatric populations.

Purpose of the Study:

  • To investigate and compare the mutation profiles within the BCP and precore regions of the HBV genome across different HBV genotypes in chronically infected children.
  • To identify genotype-specific mutation patterns in pediatric HBV infections.

Main Methods:

  • A cohort study involving 245 chronically infected children and 92 infected adults.
  • Analysis of BCP and precore regions using Polymerase Chain Reaction (PCR) amplification followed by sequencing.

Main Results:

  • Significantly higher mutation frequencies at ten nucleotide positions (nt1679, nt1721, nt1753, nt1757, nt1758, nt1762, nt1764, nt1775, nt1856, nt1858) were observed in genotype C subjects compared to genotype B subjects among children.
  • In contrast, only three positions (nt1679, nt1758, nt1775) showed higher mutation frequencies in genotype C adults versus genotype B adults.
  • Several combined mutations, including a novel triple mutation (G1721A/A1775G/T1858C), were highly prevalent in children with genotype C infection and were exclusively detected in this group.
  • The G1721A/A1775G/T1858C mutation was associated with higher viral load and a younger age distribution in the pediatric cohort.

Conclusions:

  • The mutation ratio difference between HBV genotypes B and C is more pronounced in children than in adults.
  • Specific combined mutations in the BCP and precore regions were uniquely identified in children with chronic HBV genotype C infection.
  • These pediatric-specific mutations are associated with increased viral load, highlighting potential implications for disease management in children.
Abstract

Keywords:
ChildrenGenotypeHepatitis B VirusMutation

More Related Videos

Development of a Hepatitis B Virus Reporter System to Monitor the Early Stages of the Replication Cycle09:35

Development of a Hepatitis B Virus Reporter System to Monitor the Early Stages of the Replication Cycle

Published on: February 1, 2017

14.1K
A Competent Hepatocyte Model Examining Hepatitis B Virus Entry through Sodium Taurocholate Cotransporting Polypeptide as a Therapeutic Target11:34

A Competent Hepatocyte Model Examining Hepatitis B Virus Entry through Sodium Taurocholate Cotransporting Polypeptide as a Therapeutic Target

Published on: May 10, 2022

2.8K

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.
63
Mechanisms of Retrovirus-induced Cancers01:51

Mechanisms of Retrovirus-induced Cancers

Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...
7.3K
Mechanisms of Retrovirus-induced Cancers01:51

Mechanisms of Retrovirus-induced Cancers

3.2K
The Eukaryotic Promoter Region02:40

The Eukaryotic Promoter Region

The eukaryotic promoter region is a segment of DNA located upstream of a gene. It contains an RNA polymerase binding site, a transcription start site, and several cis-regulatory sequences.  The proximal promoter region is located in the vicinity of the gene and has cis-regulatory sequences and the core promoter. The core promoter is the binding site for RNA polymerase and is usually located between -35 and +35 nucleotides from the transcription start site. The distal promoter regions are...
19.8K
The Eukaryotic Promoter Region02:40

The Eukaryotic Promoter Region

4.4K
Retroviruses02:33

Retroviruses

Retroviruses and retrotransposons both insert copies of their genetic elements into the genome of the host cell. Thus, the viral genes are passed on when the host genome is replicated or translated. A typical retroviral DNA sequence contains 3-4 genes that encode the different proteins required for its structural assembly and function as a molecular parasite. This DNA is transcribed into a single mRNA, which is very similar in structure to conventional mRNAs, i.e., it is capped at the 5’...
16.2K