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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...
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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...
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Diphtheria is an acute, toxin-mediated infectious disease that primarily affects the upper respiratory tract. It is caused by Corynebacterium diphtheriae, a Gram-positive, pleomorphic rod that lacks spore-forming capability and exhibits a characteristic club-shaped morphology under microscopic examination. While C. diphtheriae can asymptomatically colonize mucosal surfaces, clinical disease manifests only when the bacterial strain is lysogenized by a specific β-corynephage. This phage...
Cirrhosis I: Introduction01:23

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Cirrhosis is a chronic, irreversible liver disease characterized by the widespread replacement of healthy liver tissue with fibrotic scar tissue and the formation of regenerative nodules.Etiology of cirrhosisCirrhosis results from sustained liver injury that triggers progressive fibrosis and structural remodeling. The underlying causes are diverse, encompassing common and less frequent clinical conditions. Regardless of the origin, all causes lead to chronic inflammation, hepatocyte loss, and...
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A Cell Culture Model for Producing High Titer Hepatitis E Virus Stocks
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Published on: June 26, 2020

Hepatitis D: clinical features and therapy.

Mario Rizzetto1

  • 1Department of Gastroenterology, Molinette, University of Torino, Torino, Italy. mrizzetto@molinette.piemonte.it

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

Hepatitis D virus (HDV) infection, though declining, persists in Europe due to older and migrating populations. Current therapies are limited, highlighting the need for new treatments targeting HDV assembly.

Area of Science:

  • Hepatology
  • Virology
  • Infectious Diseases

Background:

  • Hepatitis D virus (HDV) infection is a significant global health concern, often leading to severe, progressive chronic liver disease.
  • HDV requires the hepatitis B virus (HBV) for its replication and spread, making HBV control crucial for HDV reduction.

Purpose of the Study:

  • To review the current epidemiological status of HDV in Europe.
  • To discuss the challenges in treating HDV infection.
  • To identify potential therapeutic targets for HDV.

Main Methods:

  • Review of epidemiological data on HDV prevalence.
  • Analysis of clinical characteristics of chronic HDV infection.
  • Discussion of current and potential therapeutic strategies for HDV.

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Stem Cell-Derived Viral Ag-Specific T Lymphocytes Suppress HBV Replication in Mice
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Stem Cell-Derived Viral Ag-Specific T Lymphocytes Suppress HBV Replication in Mice

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Main Results:

  • HDV circulation has decreased due to HBV control measures but remains endemic in Europe.
  • Two main reservoirs of HDV persist: an aging population with past infections and young migrating individuals.
  • Existing therapies for HDV are limited, with interferon showing minimal efficacy.

Conclusions:

  • Therapeutic options for HDV remain limited, necessitating novel treatment approaches.
  • The virion assembly process presents a promising target for future antiviral therapies against HDV.