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

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...
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...
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...
Immune Response Against Viral Pathogens01:29

Immune Response Against Viral Pathogens

The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
NK Cells
NK cells are a crucial part of our innate immune system, acting as the first line of defense against viral infections. These cells can recognize and kill infected cells without prior exposure to the virus, effectively slowing down the spread of infection. Additionally, NK cells produce proinflammatory...
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...
Cirrhosis II: Pathophysiology01:24

Cirrhosis II: Pathophysiology

Cirrhosis is a progressive chronic liver injury caused by prolonged inflammation, excessive fibrotic remodeling, and impaired regeneration. Over time, repeated hepatic insults disrupt the liver’s architecture and function, leading to reduced blood flow, impaired bile drainage, and diminished metabolic capacity.Pathophysiology of cirrhosisCirrhosis arises from three main responses to chronic liver damage: inflammation, immune activation, and hepatocyte death. These processes lead to structural...

You might also read

Related Articles

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

Sort by
Same author

HIV-1 envelope glycoprotein modulates CXCR4 clustering and dynamics on the T cell membrane.

eLife·2026
Same author

Discovery and SAR studies of antiviral 4-aminopiperidine derivatives active against SARS-CoV-2.

European journal of medicinal chemistry·2025
Same author

Expanding the chemical space for antiviral discovery: the potential of twistenediones.

RSC medicinal chemistry·2025
Same author

Dynamic Cellular Proteome Remodeling during SARS-CoV-2 Infection. Identification of Plasma Protein Readouts.

Journal of proteome research·2024
Same author

Preclinical evaluation of therapeutic vaccines for chronic hepatitis B that stimulate antiviral activities of T cells and NKT cells.

JHEP reports : innovation in hepatology·2024
Same author

SARS-CoV-2 membrane protein-specific antibodies from critically ill SARS-CoV-2-infected individuals interact with Fc receptor-expressing cells but do not neutralize the virus.

Journal of leukocyte biology·2024

Related Experiment Video

Updated: Jun 17, 2026

A High Resolution Method to Monitor Phosphorylation-dependent Activation of IRF3
11:44

A High Resolution Method to Monitor Phosphorylation-dependent Activation of IRF3

Published on: January 24, 2016

Hepatitis C virus blocks interferon effector function by inducing protein kinase R phosphorylation.

Urtzi Garaigorta1, Francis V Chisari

  • 1Department of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA 92037, USA. ugaraig@scripps.edu

Cell Host & Microbe
|December 17, 2009
PubMed
Summary

Hepatitis C virus (HCV) activates PKR, inhibiting interferon-stimulated gene (ISG) protein production. Suppressing PKR restores ISG expression and enhances antiviral effects, revealing a viral strategy to evade immune responses.

More Related Videos

A Protocol for Analyzing Hepatitis C Virus Replication
13:04

A Protocol for Analyzing Hepatitis C Virus Replication

Published on: June 26, 2014

Zika Virus Infectious Cell Culture System and the In Vitro Prophylactic Effect of Interferons
09:11

Zika Virus Infectious Cell Culture System and the In Vitro Prophylactic Effect of Interferons

Published on: August 23, 2016

Related Experiment Videos

Last Updated: Jun 17, 2026

A High Resolution Method to Monitor Phosphorylation-dependent Activation of IRF3
11:44

A High Resolution Method to Monitor Phosphorylation-dependent Activation of IRF3

Published on: January 24, 2016

A Protocol for Analyzing Hepatitis C Virus Replication
13:04

A Protocol for Analyzing Hepatitis C Virus Replication

Published on: June 26, 2014

Zika Virus Infectious Cell Culture System and the In Vitro Prophylactic Effect of Interferons
09:11

Zika Virus Infectious Cell Culture System and the In Vitro Prophylactic Effect of Interferons

Published on: August 23, 2016

Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Hepatitis C virus (HCV) infection induces antiviral interferon-stimulated genes (ISGs) but persists, indicating a mechanism to counteract host defenses.
  • HCV utilizes an internal ribosome entry site (IRES) for translation of its polyprotein.

Purpose of the Study:

  • To investigate how HCV evades the host's interferon-stimulated gene (ISG) antiviral response.
  • To elucidate the role of RNA-dependent protein kinase (PKR) in HCV's evasion strategy.

Main Methods:

  • Analyzing the effect of HCV infection on PKR activation and its impact on eukaryotic translation initiation factor eIF2 alpha phosphorylation.
  • Assessing ISG mRNA and protein expression levels in HCV-infected cells with and without PKR suppression.
  • Comparing host protein translation with HCV IRES-dependent translation under PKR activation.

Main Results:

  • HCV infection activates PKR, leading to eIF2 alpha phosphorylation and reduced ISG protein synthesis despite normal ISG mRNA levels.
  • Suppression of PKR in interferon-treated, HCV-infected cells restored ISG protein induction and enhanced interferon's antiviral efficacy.
  • Activated PKR inhibited host protein translation, including ISGs, but did not affect HCV IRES-driven translation.

Conclusions:

  • HCV activates PKR as a mechanism to suppress the translation of antiviral ISG proteins, thereby evading the host interferon response.
  • This PKR activation paradoxically benefits HCV by selectively inhibiting host antiviral protein synthesis while allowing viral translation to proceed.