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...

You might also read

Related Articles

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

Sort by
Same author

Structures of hepatitis B virus subviral particles and identification of potential druggable pockets for the discovery of antiviral agents.

Antiviral research·2026
Same author

HBV capsid assembly modulators differentially modulate the assembly of wild-type and drug-resistant core protein chimeric nucleocapsids and empty capsids.

PLoS pathogens·2025
Same author

Modes of action of a small molecule antiviral compound targeting yellow fever virus NS4B protein.

Proceedings of the National Academy of Sciences of the United States of America·2025
Same author

New potent HBV replication inhibitors for the management of chronic hepatitis B are needed.

Nature reviews. Gastroenterology & hepatology·2025
Same author

A Particle Gel Assay for Detection of Intracellular Hepatitis B Virus Subviral Particles in Cultured Cells.

Methods in molecular biology (Clifton, N.J.)·2024
Same author

Discovery of hepatitis B virus subviral particle biogenesis inhibitors from a bioactive compound library.

Antiviral research·2024

Related Experiment Video

Updated: May 7, 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

18.3K

Computational Approaches to Predict Hepatitis B Virus Capsid Protein Mutations That Confer Resistance to Capsid

Gideon Tolufashe1, Usha Viswanathan1, John Kulp1

  • 1Baruch S. Blumberg Institute, 3805 Old Easton Road, Doylestown, PA 18902, USA.

Viruses
|March 27, 2025
PubMed
Summary

Capsid assembly modulators (CAMs) are new antiviral drugs for chronic hepatitis B. Computational methods can predict drug resistance mutations, aiding in designing new CAMs with higher resistance barriers.

Keywords:
MM/GBSAcapsidcapsid assembly modulatorsdrug resistancehepatitis B virusmolecular dockingmolecular dynamics simulations

More Related Videos

Identifying Inhibitors of the HBx-DDB1 Interaction Using a Split Luciferase Assay System
05:55

Identifying Inhibitors of the HBx-DDB1 Interaction Using a Split Luciferase Assay System

Published on: December 21, 2019

6.6K
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

2.1K

Related Experiment Videos

Last Updated: May 7, 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

18.3K
Identifying Inhibitors of the HBx-DDB1 Interaction Using a Split Luciferase Assay System
05:55

Identifying Inhibitors of the HBx-DDB1 Interaction Using a Split Luciferase Assay System

Published on: December 21, 2019

6.6K
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

2.1K

Area of Science:

  • Virology
  • Drug Discovery
  • Computational Chemistry

Background:

  • Capsid assembly modulators (CAMs) are novel antiviral agents targeting chronic hepatitis B virus (HBV) replication.
  • CAMs function by binding to the HBV capsid protein's hydrophobic pocket, disrupting assembly and leading to non-infectious viral particles.
  • The emergence of CAM-resistant HBV variants poses a significant challenge to antiviral therapy, necessitating the development of agents with high resistance barriers.

Purpose of the Study:

  • To establish computational approaches for predicting capsid protein (Cp) mutations that confer resistance to CAMs.
  • To investigate the interaction between representative CAM-A and CAM-E compounds (BAY 41-4109 and JNJ-56136379) and wild-type and mutant HBV Cp residues within the HAP pocket.
  • To evaluate the accuracy of molecular docking, MM/GBSA, and MD simulations in predicting CAM resistance and sensitivity.

Main Methods:

  • Utilized molecular docking, MM/GBSA, and MD simulations to analyze interactions between CAMs and HBV Cp.
  • Investigated 35 naturally occurring Cp mutations at the HAP pocket using nine publicly available HBV capsid or CpY132A hexamer structures.
  • Assessed the predictive accuracy of computational methods for known resistance and sensitivity profiles.

Main Results:

  • Molecular docking accurately predicted resistance/sensitivity for over 50% of mutations for JNJ-56136379 using specific HBV capsid structures (5D7Y, 5T2P-FA).
  • MM/GBSA demonstrated over 50% accuracy in predicting resistance/sensitivity for BAY 41-4109 and JNJ-56136379 with relevant structures (5E0I-BC, 5WRE-FA, 5E0I-FA).
  • Accurate prediction of CAM resistance is achievable only when using capsid structures bound to CAMs with similar chemical scaffolds.

Conclusions:

  • Computational methods like molecular docking and MM/GBSA can predict HBV CAM resistance mutations.
  • The accuracy of these predictive models is dependent on the structural similarity between the CAM used in the simulation and the CAM under investigation.
  • These findings provide a basis for rational drug design of novel CAMs with improved resistance profiles for hepatitis B treatment.