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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...
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...
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...
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...
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...
The Proteasome01:13

The Proteasome

Eukaryotic cells can degrade proteins through several pathways. One of the most important among these is the ubiquitin-proteasome pathway. It helps the cell eliminate the misfolded, damaged, or unwarranted cytoplasmic proteins in a highly specific manner.
In this pathway, the target proteins are first tagged with small proteins called ubiquitin. This involves participation of a series of enzymes including— E1 (ubiquitin-activating enzyme), E2 (ubiquitin-conjugating enzyme), and E3 (ubiquitin...

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Related Experiment Video

Updated: May 23, 2026

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

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Published on: February 1, 2017

Hepatitis E virus replication requires an active ubiquitin-proteasome system.

Yogesh A Karpe1, Xiang-Jin Meng

  • 1Department of Biomedical Sciences and Pathobiology, College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Blacksburg, Virginia, USA.

Journal of Virology
|March 23, 2012
PubMed
Summary

Hepatitis E virus (HEV) replication needs an active ubiquitin-proteasome system. Proteasome inhibitors block HEV replication, suggesting this machinery is a potential therapeutic target.

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Published on: June 26, 2020

Area of Science:

  • Virology
  • Molecular Biology
  • Cellular Biology

Background:

  • The replication mechanism of the Hepatitis E virus (HEV) is not well understood.
  • Identifying key host factors involved in HEV replication is crucial for developing antiviral strategies.

Purpose of the Study:

  • To investigate the role of the ubiquitin-proteasome system (UPS) in HEV replication.
  • To explore the potential of targeting the UPS as a therapeutic strategy against HEV infection.

Main Methods:

  • Utilized proteasome inhibitors to assess their impact on HEV replication.
  • Examined viral transcription and translation in the presence of inhibitors.
  • Investigated the effect of ubiquitin overexpression on HEV replication in inhibitor-treated cells.

Main Results:

  • HEV replication was found to be dependent on an active ubiquitin-proteasome system.
  • Proteasome inhibitors significantly impaired HEV replication, likely by inhibiting viral transcription and/or translation.
  • Cellular translation remained largely unaffected by the proteasome inhibitors.
  • Overexpression of ubiquitin partially rescued HEV replication in cells treated with proteasome inhibitors.

Conclusions:

  • The ubiquitin-proteasome system is essential for Hepatitis E virus replication.
  • HEV replication involves interactions with the host cell's proteasome machinery.
  • Targeting the proteasome system represents a promising therapeutic avenue for treating HEV infections.