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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...
Mechanisms of Retrovirus-induced Cancers01:51

Mechanisms of Retrovirus-induced Cancers

Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...
Mechanisms of Retrovirus-induced Cancers01:51

Mechanisms of Retrovirus-induced Cancers

Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...
Mutagenicity and Carcinogenicity01:25

Mutagenicity and Carcinogenicity

Mutagenicity and carcinogenicity refer to the ability of drugs to cause genetic defects and induce cancer, respectively. The International Agency for Research on Cancer (IARC) classifies agents into four groups based on their carcinogenic potential. Group 1 agents are known human carcinogens; group 2A agents are probably carcinogenic to humans; group 3 agents lack data to support their role in carcinogenesis; and group 4 includes agents for which data support that they are not likely to be...
Rous Sarcoma Virus (RSV) and Cancer01:03

Rous Sarcoma Virus (RSV) and Cancer

Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
RSV is a retrovirus that contains two copies of a plus-strand  RNA genome. Its genome consists of four main open...

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Related Experiment Video

Updated: Jul 3, 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 B virus and hepatocarcinogenesis.

Faisal Azam1, Anastasios Koulaouzidis

  • 1Department of Oncology, Glan Clwyd Hospital, Rhyl, UK. drfaisalazam@hotmail.co.uk

Annals of Hepatology
|July 16, 2008
PubMed
Summary

Hepatitis B viral infection is a leading cause of liver cancer. The Hepatitis B X-protein disrupts cellular functions, playing a key role in the development of liver cancer in infected patients.

Area of Science:

  • Hepatology
  • Oncology
  • Molecular Biology

Background:

  • Hepatitis B viral (HBV) infection is a primary cause of hepatocellular carcinoma (HCC).
  • HBV DNA levels are crucial predictors of liver cancer development in patients positive for HB surface antigen.
  • Understanding the molecular mechanisms of hepatocarcinogenesis is vital for developing targeted therapies.

Purpose of the Study:

  • To review the molecular mechanisms of hepatocarcinogenesis driven by HBV infection.
  • To specifically emphasize the role of the Hepatitis B X-protein in liver cancer development.
  • To elucidate how HBV X-protein interacts with host cellular pathways.

Main Methods:

  • Literature review focusing on molecular mechanisms of HBV-induced liver cancer.

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Last Updated: Jul 3, 2026

A Competent Hepatocyte Model Examining Hepatitis B Virus Entry through Sodium Taurocholate Cotransporting Polypeptide as a Therapeutic Target
11:34

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

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Real-Time Polymerase Chain Reaction-Based Detection and Quantification of Hepatitis B Virus DNA
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Real-Time Polymerase Chain Reaction-Based Detection and Quantification of Hepatitis B Virus DNA

Published on: December 15, 2023

  • Analysis of studies detailing the function of Hepatitis B X-protein.
  • Examination of cellular processes affected by HBV X-protein.

    • Main Results:

    • Hepatitis B X-protein interacts with numerous host targets.
    • Disruption of critical cellular functions including cell cycle regulation and apoptosis by HBV X-protein.
    • Alteration of host gene expression, including oncogenes and tumor suppressor genes, by HBV X-protein.

    Conclusions:

    • Hepatitis B X-protein is a significant factor in HBV-related hepatocarcinogenesis.
    • The X-protein's interference with cellular pathways contributes to liver cancer development.
    • Targeting the molecular functions of HBV X-protein may offer therapeutic strategies for HCC.