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Hepatitis

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...

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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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Immune Response Against Viral Pathogens

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Related Experiment Video

Updated: Jul 7, 2026

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

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

Published on: June 5, 2020

Hepatitis B virus-cell interactions and pathogenesis.

David H Nguyen¹, Laurie Ludgate, Jianming Hu

¹Department of Microbiology and Immunology, The Pennsylvania State University, College of Medicine, Hershey, Pennsylvania 17033, USA.

Journal of Cellular Physiology

|February 28, 2008

Summary

This summary is machine-generated.

Hepatitis B virus (HBV) replication relies on interactions between viral and host factors within infected cells. This review details recent findings on these virus-host interactions, crucial for understanding HBV persistence and pathogenesis.

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Last Updated: Jul 7, 2026

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

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Published on: June 5, 2020

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

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Published on: May 10, 2022

Detection of Low Copy Number Integrated Viral DNA Formed by In Vitro Hepatitis B Infection

Detection of Low Copy Number Integrated Viral DNA Formed by In Vitro Hepatitis B Infection

Published on: November 7, 2018

Area of Science:

Virology
Molecular Biology
Cell Biology

Background:

Hepatitis B virus (HBV) infection is a global health concern.
Viral replication and disease pathogenesis are driven by complex virus-host interactions.
Understanding these interactions at the cellular level is key to developing antiviral strategies.

Purpose of the Study:

To review recent advancements in understanding virus-host interactions during HBV infection.
To highlight key cellular processes and factors involved in HBV replication and persistence.
To provide insights into the molecular mechanisms governing HBV pathogenesis.

Main Methods:

This review synthesizes findings from recent experimental studies.
Focuses on research investigating cellular chaperones, HBV X protein (HBx), HBV episomal DNA, and cellular factors.
Integrates data on viral entry, reverse transcription, nucleocapsid maturation, and virion secretion.

Main Results:

Cellular chaperones are essential for initiating HBV reverse transcription.
The HBV X protein (HBx) modulates viral and cellular transcription and signaling pathways.
Epigenetic regulation of HBV episomal DNA influences viral persistence.
Specific cellular factors mediate HBV entry, nucleocapsid maturation, and virion secretion.

Conclusions:

Virus-host interactions within the infected cell are critical for HBV replication and pathogenesis.
Recent progress has elucidated the roles of cellular chaperones, HBx, and epigenetic modifications.
Identifying these cellular factors offers potential targets for therapeutic intervention against HBV.