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

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...
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...
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...
Chronic Pancreatitis II: Pathophysiology01:21

Chronic Pancreatitis II: Pathophysiology

Chronic pancreatitis is a progressive and irreversible inflammation of the pancreas, most often caused by long-term alcohol abuse, but it can also be related to ductal obstruction, smoking, or genetic factors.Chronic pancreatitis occurs when the pancreas is repeatedly exposed to harmful agents like alcohol, smoking, ductal obstruction, or genetic predisposition. These factors lead to the release of toxic metabolites and inflammatory cytokines, sustaining chronic inflammation in the pancreatic...
Acute Pancreatitis II: Clinical Manifestations and Management01:30

Acute Pancreatitis II: Clinical Manifestations and Management

Acute pancreatitis presents a complex medical emergency characterized by rapid onset inflammation of the pancreas, demanding timely diagnosis and management to prevent complications. The condition primarily manifests through severe upper abdominal pain that often radiates to the back. This pain intensifies following the consumption of fatty foods. Accompanying symptoms such as nausea, vomiting, abdominal distention, fever, dyspnea, cyanosis, and jaundice can vary in intensity but significantly...
Acute Pancreatitis II: Pathophysiology01:21

Acute Pancreatitis II: Pathophysiology

The pathophysiology of acute pancreatitis centers on injury to pancreatic acinar cells, which initiates a cascade of harmful intracellular events.This injury leads to premature activation of trypsinogen to trypsin in the pancreas. Trypsin then activates other digestive enzymes, such as chymotrypsin, elastase, and phospholipase A2, which begin breaking down pancreatic tissue. The resulting autodigestion causes local inflammation, tissue swelling, hemorrhage, and fat necrosis.Injured acinar cells...

You might also read

Related Articles

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

Sort by
Same author

FIB-4 and APRI as Predictive Factors for Short- and Long-Term Survival in Patients with Transjugular Intrahepatic Portosystemic Stent Shunts.

Biomedicines·2022
Same author

Clinical and biochemical endpoints and predictors of response to plasma exchange in septic shock: results from a randomized controlled trial.

Critical care (London, England)·2022
Same author

Impact on follow-up strategies in patients with primary sclerosing cholangitis.

Liver international : official journal of the International Association for the Study of the Liver·2022
Same author

Out of sight for the endoscopist? Gastrointestinal bleeding after aortic repair.

Scandinavian journal of gastroenterology·2022
Same author

Elevated fractional donor-derived cell-free DNA during subclinical graft injury after liver transplantation.

Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society·2022
Same author

Correction: Safety and efficacy of prophylactic and therapeutic vaccine based on live-attenuated Listeria monocytogenes in hepatobiliary cancers.

Oncogene·2022

Related Experiment Video

Updated: Jun 13, 2026

The CYP2D6 Animal Model: How to Induce Autoimmune Hepatitis in Mice
09:03

The CYP2D6 Animal Model: How to Induce Autoimmune Hepatitis in Mice

Published on: February 3, 2012

Hepatitis delta: immunopathogenesis and clinical challenges.

Jan Grabowski1, Heiner Wedemeyer

  • 1Department of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover, Germany.

Digestive Diseases (Basel, Switzerland)
|May 13, 2010
PubMed
Summary

Hepatitis delta, the most severe viral hepatitis, is caused by the hepatitis D virus (HDV) in those with hepatitis B virus (HBV). Chronic HDV infection accelerates liver disease and increases cancer risk, with interferon showing limited efficacy.

More Related Videos

Analysis of HBV-Specific CD4 T-cell Responses and Identification of HLA-DR-Restricted CD4 T-Cell Epitopes Based on a Peptide Matrix
10:37

Analysis of HBV-Specific CD4 T-cell Responses and Identification of HLA-DR-Restricted CD4 T-Cell Epitopes Based on a Peptide Matrix

Published on: October 20, 2021

Induction of Drug-Induced, Autoimmune Hepatitis in BALB/c Mice for the Study of Its Pathogenic Mechanisms
11:36

Induction of Drug-Induced, Autoimmune Hepatitis in BALB/c Mice for the Study of Its Pathogenic Mechanisms

Published on: May 29, 2020

Related Experiment Videos

Last Updated: Jun 13, 2026

The CYP2D6 Animal Model: How to Induce Autoimmune Hepatitis in Mice
09:03

The CYP2D6 Animal Model: How to Induce Autoimmune Hepatitis in Mice

Published on: February 3, 2012

Analysis of HBV-Specific CD4 T-cell Responses and Identification of HLA-DR-Restricted CD4 T-Cell Epitopes Based on a Peptide Matrix
10:37

Analysis of HBV-Specific CD4 T-cell Responses and Identification of HLA-DR-Restricted CD4 T-Cell Epitopes Based on a Peptide Matrix

Published on: October 20, 2021

Induction of Drug-Induced, Autoimmune Hepatitis in BALB/c Mice for the Study of Its Pathogenic Mechanisms
11:36

Induction of Drug-Induced, Autoimmune Hepatitis in BALB/c Mice for the Study of Its Pathogenic Mechanisms

Published on: May 29, 2020

Area of Science:

  • Hepatology
  • Virology
  • Immunology

Background:

  • Hepatitis delta is caused by the hepatitis D virus (HDV), requiring hepatitis B virus (HBV) surface antigen for replication.
  • HDV infection is the most severe form of viral hepatitis, leading to accelerated liver disease progression.
  • Eight distinct HDV genotypes exist, each with unique geographic distributions and clinical implications.

Purpose of the Study:

  • To summarize the clinical significance and treatment landscape of hepatitis delta.
  • To highlight the severe outcomes of chronic HDV infection compared to HBV monoinfection.
  • To discuss current and potential future therapeutic strategies for HDV.

Main Methods:

  • Review of existing literature on HDV epidemiology, pathogenesis, and clinical course.
  • Analysis of treatment outcomes for interferon-based therapies.
  • Exploration of emerging therapeutic targets and immune response studies.

Main Results:

  • Chronic HDV infection results in more severe liver disease, including faster fibrosis progression and earlier decompensation.
  • Hepatic decompensation is the primary clinical endpoint, contrasting with liver cancer in HCV infection.
  • Interferon-alpha offers antiviral activity, with pegylated interferon achieving sustained virological response in approximately 25% of patients.

Conclusions:

  • Hepatitis delta represents a severe liver disease with significant morbidity and mortality.
  • Interferon-based treatments provide some benefit, but novel therapies are needed.
  • Further research into HDV-specific immune responses is crucial for developing effective treatments.