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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...
Receptor-mediated Endocytosis01:20

Receptor-mediated Endocytosis

Receptor-mediated endocytosis is when bulk amounts of specific molecules are imported into a cell after binding to cell surface receptors. The molecules bound to these receptors are taken into the cell through inward folding of the cell surface membrane, which is eventually pinched off into a vesicle within the cell. Structural proteins, such as clathrin, coat the budding vesicle.
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Receptor-mediated Endocytosis01:38

Receptor-mediated Endocytosis

Overview
Receptor-Mediated Endocytosis01:20

Receptor-Mediated Endocytosis

Receptor-mediated endocytosis is when bulk amounts of specific molecules are imported into a cell after binding to cell surface receptors. The molecules bound to these receptors are taken into the cell through inward folding of the cell surface membrane, which is eventually pinched off into a vesicle within the cell. Structural proteins, such as clathrin, coat the budding vesicle.
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Cytomegalovirus Disease01:27

Cytomegalovirus Disease

Cytomegalovirus (CMV) disease is caused by human cytomegalovirus, a double-stranded DNA virus of the Herpesviridae family. While primary CMV infection is often asymptomatic in immunocompetent individuals, the virus can cause severe disease in neonates and immunocompromised patients. CMV is the most common cause of congenital viral infection in the United States, and a major pathogen in solid organ and hematopoietic stem cell transplant recipients.CMV is transmitted via bodily fluids, sexual...

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Related Experiment Video

Updated: May 24, 2026

A Competent Hepatocyte Model Examining Hepatitis B Virus Entry through Sodium Taurocholate Cotransporting Polypeptide as a Therapeutic Target
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A Competent Hepatocyte Model Examining Hepatitis B Virus Entry through Sodium Taurocholate Cotransporting Polypeptide as a Therapeutic Target

Published on: May 10, 2022

Hepatitis C virus entry: beyond receptors.

Luke W Meredith1, Garrick K Wilson, Nicola F Fletcher

  • 1Institute for Biomedical Research, University of Birmingham, Birmingham, UK.

Reviews in Medical Virology
|March 7, 2012
PubMed
Summary
This summary is machine-generated.

Hepatitis C virus (HCV) entry into liver cells involves multiple host factors, including CD81 and claudin-1. Targeting these viral entry mechanisms offers promising therapeutic strategies for treating HCV infection.

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Last Updated: May 24, 2026

A Competent Hepatocyte Model Examining Hepatitis B Virus Entry through Sodium Taurocholate Cotransporting Polypeptide as a Therapeutic Target
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Two Methods of Heterokaryon Formation to Discover HCV Restriction Factors
16:49

Two Methods of Heterokaryon Formation to Discover HCV Restriction Factors

Published on: July 16, 2012

Area of Science:

  • Hepatology
  • Virology
  • Molecular Biology

Background:

  • Hepatitis C virus (HCV) is a significant global health concern, causing progressive liver disease in approximately 3% of the world's population.
  • HCV infection is a blood-borne viral disease with complex pathogenesis.
  • Understanding HCV pathogenesis is crucial for developing effective treatments.

Purpose of the Study:

  • To review recent literature on Hepatitis C virus (HCV) entry mechanisms.
  • To identify host cell molecules essential for HCV entry.
  • To explore the potential for therapeutic interventions targeting HCV entry.

Main Methods:

  • Review of recent scientific literature on HCV entry.
  • Identification of key host cell receptors involved in HCV entry, including tetraspanin CD81, scavenger receptor B1, claudin-1, and occludin.
  • Analysis of emerging evidence on additional factors, such as inflammatory mediators, influencing HCV entry.

Main Results:

  • HCV entry is a complex, multi-step process dependent on specific host cell molecules.
  • Tetraspanin CD81, scavenger receptor B1, claudin-1, and occludin are essential for HCV entry.
  • Inflammatory mediators and other factors beyond classical receptors also regulate hepatocyte susceptibility to HCV.

Conclusions:

  • The receptor-dependent nature of HCV entry presents a viable target for therapeutic strategies.
  • Additional host factors regulating HCV entry may offer novel avenues for drug design.
  • Targeting HCV entry mechanisms holds significant potential for future treatment and drug development.