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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...
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...
Yellow Fever01:18

Yellow Fever

Yellow fever is a viral hemorrhagic disease caused by the yellow fever virus (YFV), a member of the Flaviviridae family. It is transmitted primarily by Aedes and Haemagogus mosquitoes in tropical and subtropical regions of Africa and South America. After transmission through a mosquito bite, the virus initially replicates in skin-resident immune cells such as dendritic cells and macrophages. These cells then migrate to the lymph nodes, where viral replication increases, eventually leading to...
Cirrhosis I: Introduction01:23

Cirrhosis I: Introduction

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...
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...
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...

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Related Experiment Video

Updated: Jun 5, 2026

A Cell Culture Model for Producing High Titer Hepatitis E Virus Stocks
10:28

A Cell Culture Model for Producing High Titer Hepatitis E Virus Stocks

Published on: June 26, 2020

Hepatitis delta virus infection: open issues.

Grazia Anna Niro1, Domenica Gioffreda, Rosanna Fontana

  • 1Gastroenterology Unit, IRCCS Casa Sollievo della Sofferenza, San Giovanni Rotondo, Italy. g.niro@operapadrepio.it

Digestive and Liver Disease : Official Journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
|January 4, 2011
PubMed
Summary

Hepatitis delta virus (HDV) replication relies on host enzymes, not its own polymerase. Understanding HDV genotypes and improving detection methods like PCR are key for developing new antiviral strategies against this infection.

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Modeling Hepatitis B Virus Infection in Non-Hepatic 293T-NE-3NRs Cells

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Last Updated: Jun 5, 2026

A Cell Culture Model for Producing High Titer Hepatitis E Virus Stocks
10:28

A Cell Culture Model for Producing High Titer Hepatitis E Virus Stocks

Published on: June 26, 2020

Modeling Hepatitis B Virus Infection in Non-Hepatic 293T-NE-3NRs Cells
09:02

Modeling Hepatitis B Virus Infection in Non-Hepatic 293T-NE-3NRs Cells

Published on: June 5, 2020

Area of Science:

  • Virology
  • Molecular Biology
  • Hepatology

Background:

  • Hepatitis delta virus (HDV) is a circular, single-stranded RNA virus requiring host cell machinery for replication.
  • HDV replication mechanisms are not fully understood, hindering the development of targeted antiviral therapies.
  • Eight distinct HDV genotypes exist, showing significant nucleotide sequence variation (up to 40%).

Purpose of the Study:

  • To elucidate the replication mechanisms of Hepatitis delta virus.
  • To highlight the importance of genomic variability and detection techniques for HDV research.
  • To inform the development of novel antiviral strategies against HDV infection.

Main Methods:

  • Cloning of HDV-RNA to create genetic probes for detection.
  • Application of reverse transcriptase-polymerase chain reaction (RT-PCR) for enhanced HDV-RNA sensitivity.
  • Development of home-made assays for HDV-RNA quantification in serum and liver.

Main Results:

  • RT-PCR significantly improved the sensitivity of HDV-RNA detection.
  • Standardized commercial tests for viral load are lacking; assays vary between centers.
  • Real-time PCR quantification of HDV in serum is a recent advancement for managing chronic infections.

Conclusions:

  • Further understanding of HDV replication is crucial for antiviral development.
  • Improved detection and quantification methods, like real-time PCR, aid in managing HDV infections.
  • Current Hepatitis B virus (HBV) inhibitors show limited efficacy against HDV replication.