Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Pharmacogenomics: Identification of New Drug Targets

Pharmacogenomics: Identification of New Drug Targets

Advances in genomics have profoundly influenced drug discovery by increasing both the speed and accuracy of pharmaceutical development. Pharmacogenomics, which examines how genetic variation influences drug response, facilitates the identification of novel therapeutic targets and enables patient stratification for personalized treatment. These strategies contribute to improved drug efficacy, minimized adverse effects, and more efficient clinical trial design.Mapping genetic differences...

Hepatitis

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: Introduction

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...

You might also read

Related Articles

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

Sort by

Same author

Hospital-Admitted Injection-Related Infections Among Incarcerated People Who Inject Drugs in Australia: A Retrospective Cohort Study.

The Medical journal of Australia·2026

Same author

Impact of bariatric surgery on alcohol-use disorder and alcohol-related liver disease: A retrospective study.

Addiction (Abingdon, England)·2026

Same author

C no more: a prospective single-arm study to evaluate the effectiveness of a nurse and peer-led mobile model of hepatitis C testing and treatment at community corrections offices.

Health & justice·2026

Same author

Reflex Testing for Hepatitis D Infection: A Unique Opportunity to Reduce Hepatitis D-Related Chronic Liver Disease Deaths in Australia.

The Medical journal of Australia·2026

Same author

The diagnosis and management of portal hypertension in cirrhosis: The Gastroenterological Society of Australia consensus.

Hepatology communications·2026

Same author

A Costing Analysis of a Nurse- and Peer-Led Mobile Model of Hepatitis C Care Adjacent to the Community Corrections Setting.

Open forum infectious diseases·2026

Search research articles

Related Experiment Video

Updated: May 29, 2026

A Protocol for Analyzing Hepatitis C Virus Replication

A Protocol for Analyzing Hepatitis C Virus Replication

Published on: June 26, 2014

Host genomics and HCV treatment response.

Paul J Clark¹, Alexander J Thompson

¹Duke Clinical Research Institute, Duke University Medical Center, Durham, North Carolina, USA.

Journal of Gastroenterology and Hepatology

|September 16, 2011

Summary

The interleukin-28B (IL28B) polymorphism influences hepatitis C virus (HCV) clearance and treatment response. This review examines IL28B

Area of Science:

Genetics
Hepatology
Virology

Background:

The interleukin-28B (IL28B) polymorphism was identified in 2009 as a significant factor influencing hepatitis C virus (HCV) infection outcomes.
Over 100 studies have since explored the IL28B polymorphism's role in HCV, yet clinical and mechanistic questions persist.

Purpose of the Study:

To review the association between IL28B variants and HCV treatment response and spontaneous clearance.
To explore the biological mechanisms and clinical implications of IL28B polymorphisms in various HCV contexts.
To assess the relevance of IL28B in the era of direct-acting antivirals.

Main Methods:

Review of peer-reviewed literature on IL28B polymorphism and HCV.
Discussion of genome-wide association study (GWAS) methodologies.

More Related Videos

Generation and Single-Cell Transcriptomic Analysis of Hepatocellular Carcinoma Organoids following Drug Treatment

Generation and Single-Cell Transcriptomic Analysis of Hepatocellular Carcinoma Organoids following Drug Treatment

Published on: May 26, 2026

Two Methods of Heterokaryon Formation to Discover HCV Restriction Factors

Two Methods of Heterokaryon Formation to Discover HCV Restriction Factors

Published on: July 16, 2012

Related Experiment Videos

Last Updated: May 29, 2026

A Protocol for Analyzing Hepatitis C Virus Replication

A Protocol for Analyzing Hepatitis C Virus Replication

Published on: June 26, 2014

Generation and Single-Cell Transcriptomic Analysis of Hepatocellular Carcinoma Organoids following Drug Treatment

Generation and Single-Cell Transcriptomic Analysis of Hepatocellular Carcinoma Organoids following Drug Treatment

Published on: May 26, 2026

Two Methods of Heterokaryon Formation to Discover HCV Restriction Factors

Two Methods of Heterokaryon Formation to Discover HCV Restriction Factors

Published on: July 16, 2012

Analysis of IL28B's relevance in different HCV genotypes, co-infections, and post-transplant settings.

Main Results:

IL28B variants significantly impact interferon-based treatment response and spontaneous clearance in genotype 1 HCV.
The polymorphism's influence extends to non-genotype 1 HCV, HIV/HCV co-infection, and recurrent HCV post-transplantation.
Biological mechanisms involve regulation of interferon-stimulated gene expression in the liver.

Conclusions:

IL28B polymorphism remains a key genetic factor in understanding HCV infection dynamics.
Further research is needed to fully elucidate mechanisms and clinical applications.
The relevance of IL28B needs re-evaluation with the advent of direct-acting antivirals (DAAs).