Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

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...
Transducer Mechanism: Nuclear Receptors01:31

Transducer Mechanism: Nuclear Receptors

Nuclear receptors, or NRs, are unique transcription factors that regulate gene transcription and affect the cellular pathways involved in reproduction, development, or metabolism. Their ability to be stimulated by small lipophilic ligands and control vital cellular processes makes them ideal drug targets. Nearly 10-15% of currently prescribed drugs target these receptors.
About 48 different soluble family members of nuclear receptors are identified that can be divided into two main classes:
Inhibitors of Viral Protein Synthesis01:30

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...
Inhibitors Of Virion Release01:25

Inhibitors Of Virion Release

Viral replication and dissemination rely on efficient mechanisms for host cell entry, genome replication, assembly, and release. Influenza viruses, such as types A and B, are negative-sense single-stranded RNA viruses with a segmented genome, that depend on two critical surface glycoproteins to carry out these processes: hemagglutinin (HA) and neuraminidase (NA). HA initiates infection by binding to sialic acid residues on the surface of host epithelial cells, facilitating receptor-mediated...
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...
Viruses with RNA Genomes01:29

Viruses with RNA Genomes

RNA viruses are categorized into positive-strand, negative-strand, or double-stranded groups based on their genomic structure and replication mechanisms. This classification dictates how they exploit host cellular machinery for protein synthesis and replication. Some RNA viruses also utilize reverse transcription as part of their life cycle, further diversifying their replication strategies.Positive-Strand RNA VirusesPositive-strand RNA viruses have genomes that function directly as messenger...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Beyond peak wavelength: spectral bandwidth of blue and red-blue laser diodes modulates photosynthesis, canopy architecture, chlorophyll maintenance, and whole-plant growth.

Frontiers in plant science·2026
Same author

A sequentially responsive DNA nanodevice for spatioselective imaging of mitochondrial miRNA and early assessment of therapeutic efficacy.

Biosensors & bioelectronics·2026
Same author

Target-triggered assembly of engineered bacteria enables dual-mode detection of microRNA.

Biosensors & bioelectronics·2026
Same author

Hepatitis B virus covalently closed circular DNA formation in murine hepatic cells uncovers a late entry block.

Proceedings of the National Academy of Sciences of the United States of America·2026
Same author

Dual organelle targeting type I/II photosensitizer triggers ferroptosis-like/apoptosis for photodynamic immunotherapy.

Bioorganic chemistry·2026
Same author

Metal-Free Photocatalyst Photo-oxidizes NADPH to Trigger Pyropstosis and Disulfidptosis for Photocatalytic Therapy of Hypoxia Tumor.

Journal of medicinal chemistry·2026

Related Experiment Video

Updated: Jun 18, 2026

Development of a Hepatitis B Virus Reporter System to Monitor the Early Stages of the Replication Cycle
09:35

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

Published on: February 1, 2017

Multiple nuclear receptors may regulate hepatitis B virus biosynthesis during development.

Vanessa Reese1, Caitlin Ondracek, Christel Rushing

  • 1Department of Microbiology and Immunology, College of Medicine, University of Illinois at Chicago, Chicago, IL 60612-7344, USA. vreese2@uic.edu

The International Journal of Biochemistry & Cell Biology
|November 28, 2009
PubMed
Summary
This summary is machine-generated.

Hepatitis B virus (HBV) replication is controlled by the 3.5 kb pregenomic RNA transcript. Hepatocyte nuclear factor 4α (HNF4α) regulates HBV transcription and replication during neonatal liver development.

More Related Videos

Modeling Hepatitis B Virus Infection in Non-Hepatic 293T-NE-3NRs Cells
09:02

Modeling Hepatitis B Virus Infection in Non-Hepatic 293T-NE-3NRs Cells

Published on: June 5, 2020

A Competent Hepatocyte Model Examining Hepatitis B Virus Entry through Sodium Taurocholate Cotransporting Polypeptide as a Therapeutic Target
11:34

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

Published on: May 10, 2022

Related Experiment Videos

Last Updated: Jun 18, 2026

Development of a Hepatitis B Virus Reporter System to Monitor the Early Stages of the Replication Cycle
09:35

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

Published on: February 1, 2017

Modeling Hepatitis B Virus Infection in Non-Hepatic 293T-NE-3NRs Cells
09:02

Modeling Hepatitis B Virus Infection in Non-Hepatic 293T-NE-3NRs Cells

Published on: June 5, 2020

A Competent Hepatocyte Model Examining Hepatitis B Virus Entry through Sodium Taurocholate Cotransporting Polypeptide as a Therapeutic Target
11:34

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

Published on: May 10, 2022

Area of Science:

  • Hepatology
  • Virology
  • Molecular Biology

Background:

  • Hepatitis B virus (HBV) biosynthesis is primarily determined by the expression of its 3.5 kb pregenomic RNA transcript in the liver.
  • Neonatal HBV transcription is developmentally regulated by hepatocyte nuclear factor 4α (HNF4α).

Purpose of the Study:

  • To investigate the role of HNF4α in regulating HBV transcription and replication during neonatal liver development.
  • To explore the involvement of other nuclear receptors in supporting HBV biosynthesis.

Main Methods:

  • Analysis of HBV 3.5 kb pregenomic RNA transcription and replication in vivo and in non-hepatoma cells.
  • Investigating the interaction of HNF4α with the HBV nucleocapsid promoter.
  • Examining the role of other nuclear receptors, including RXRα/PPARα, RXRα/FXRα, LRH1, and ERR, in HBV replication.

Main Results:

  • HNF4α directly supports HBV biosynthesis in non-hepatoma cells.
  • HNF4α may progressively activate HBV transcription and replication by binding to the nucleocapsid promoter during neonatal liver development.
  • Additional nuclear receptors can support HBV transcription and replication in non-hepatoma cells.

Conclusions:

  • HNF4α plays a crucial role in regulating HBV biosynthesis during neonatal liver development.
  • HNF4α may act directly or indirectly through a network of liver-enriched nuclear receptors to control HBV transcription and replication.