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...
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...
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’...
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...
Amebiasis01:28

Amebiasis

Entamoeba histolytica, a protozoan parasite, is responsible for intestinal and extraintestinal amebiasis. Though a significant proportion of infections remain asymptomatic, approximately 50 million individuals annually are estimated to present with clinical disease, resulting in up to 100,000 deaths globally. The disease burden is disproportionately high in regions with lower socioeconomic status, such as parts of India, Africa, Mexico, and Latin America.Etiology and TransmissionThe infective...

You might also read

Related Articles

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

Sort by
Same author

Editorial: HIV-1 Tat, an enhancer of virus infectivity and disease promoter: target for preventive and therapeutic interventions.

Frontiers in immunology·2026
Same author

Broad-spectrum CRISPR-Cas13d-mediated strategy for combating human coronaviruses.

Molecular therapy. Nucleic acids·2026
Same author

Elucidating the kinetics of CRISPR-SaCas9 action to obtain effective HIV DNA excision with two gRNAs.

Nucleic acids research·2026
Same author

The genetic architecture of HIV-1 virulence.

Virus evolution·2025
Same author

HIV-2 evades restriction by ZAP through adaptations in the U3 LTR region despite increased CpG levels.

Nucleic acids research·2025
Same author

HIV-phyloTSI: subtype-independent estimation of time since HIV-1 infection for cross-sectional measures of population incidence using deep sequence data.

BMC bioinformatics·2025

Related Experiment Video

Updated: Jun 27, 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

Occult hepatitis B infection: an evolutionary scenario.

Formijn J van Hemert1, Hans L Zaaijer, Ben Berkhout

  • 1Department of Medical Microbiology, Laboratory of Experimental Virology, Center for Infection and Immunity Amsterdam Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands. f.j.vanhemert@amc.uva.nl

Virology Journal
|December 17, 2008
PubMed
Summary

Occult hepatitis B virus (HBV) infection may arise from a novel RNA splicing event that eliminates surface protein expression. This leads to virus accumulation within cells, driving occult HBV evolution.

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

Related Experiment Videos

Last Updated: Jun 27, 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

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

Area of Science:

  • Virology
  • Molecular Biology
  • Evolutionary Biology

Background:

  • Occult hepatitis B virus (HBV) infection is characterized by detectable HBV DNA but undetectable hepatitis B surface antigen (HBsAg).
  • The mechanisms driving the transition from overt to occult HBV infection remain poorly understood.
  • This study investigates the genetic and molecular basis of occult HBV infection using a unique blood donor case.

Purpose of the Study:

  • To elucidate the evolutionary mechanisms underlying occult hepatitis B virus infection.
  • To compare the full-length HBV genome of an occult infection case with global genotype D strains.
  • To identify genetic alterations associated with the development of occult HBV infection.

Main Methods:

  • Phylogenetic analysis of HBV polymerase, core, and X protein sequences.
  • Analysis of surface protein evolution and identification of positive selection.
  • 3D protein complex modeling to assess protein interface mutations.
  • Identification and characterization of a novel RNA splicing event (2986-202 deletion).
  • Phylogenetic analysis of genotype D HBV strains based on splicing ability.

Main Results:

  • Phylogenetic analysis did not differentiate the occult strain (d4) based on polymerase, core, or X proteins, but its surface protein formed an outgroup, indicating positive selection (dN/dS = 1.3787).
  • A novel RNA splicing event (2986-202 deletion) was identified, abolishing surface protein expression while preserving other viral functions.
  • Genotype D strains exhibit varying efficiencies in this splicing event, with prone strains forming a distinct clade.
  • A specific substitution (G173T) linked to clade membership alters RNA secondary structure, potentially affecting splicing at the 202 acceptor site.

Conclusions:

  • A proposed evolutionary pathway for occult HBV involves 2986-202 splicing, generating surface protein-deficient virions.
  • Relaxation of coding constraints in these virions leads to mutation accumulation.
  • These surface protein-deficient viruses are replication-impaired and cell-associated, contributing to occult infection persistence.