Related Experiment Video

Updated: May 7, 2026

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

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 core protein interacts with CD59 to promote complement-mediated liver inflammation during chronic

Dong Liu1, Bing Ni, Li Wang

  • 1Institute of Immunology, PLA, The Third Military Medical University, Chongqing 400038, China.

FEBS Letters
|September 17, 2013
PubMed

Insights

Hepatitis B virus core protein (HBc) down-regulates CD59 in liver cells, increasing susceptibility to immune attack. This interaction explains liver injury in Hepatitis B virus infection.

Area of Science:

  • Immunology
  • Hepatology
  • Virology

Background:

  • Immune-mediated inflammation is a primary driver of liver injury in Hepatitis B virus (HBV) infection.
  • The Hepatitis B virus core protein (HBc) plays a role in viral pathogenesis.
  • Understanding host-pathogen interactions is crucial for developing therapeutic strategies.

Purpose of the Study:

  • To identify host proteins interacting with HBc in hepatocytes.
  • To investigate the functional consequences of HBc-host protein interactions on liver cell injury.
  • To elucidate the mechanism by which HBc influences host immune responses.

Main Methods:

  • Tandem affinity purification (TAP) screening to identify HBc-interacting proteins.
  • Cell culture models (HepG2, HepG2.215 cells) with HBc transfection.
  • Analysis of CD59 expression and localization using laser confocal microscopy, quantitative PCR, and flow cytometry.
  • Assessment of hepatocyte sensitivity to membrane attack complex (MAC)-induced lysis.

Main Results:

  • CD59 was identified as a novel HBc-interacting protein in hepatocytes.
  • HBc significantly down-regulated CD59 expression at both mRNA and protein levels.
  • CD59 translocated to the nucleus upon binding to HBc.
  • Down-regulation of CD59 increased hepatocyte sensitivity to MAC-induced lysis.
  • Accumulation of MACs was observed in the livers of HBV-infected patients, correlating with findings.

Conclusions:

  • CD59 is a key host factor involved in HBV-associated liver injury.
  • HBc-induced CD59 down-regulation enhances immune-mediated hepatocyte damage.
  • Targeting the HBc-CD59 interaction may offer a therapeutic approach for HBV infection.

Keywords:
CD59ComplementHBVHBcInflammationMAC

More Related Videos

Development of a Hepatitis B Virus Reporter System to Monitor the Early Stages of the Replication Cycle09:35

Development of a Hepatitis B Virus Reporter System to Monitor the Early Stages of the Replication Cycle

Published on: February 1, 2017

"Liver-on-a-Chip" Cultures of Primary Hepatocytes and Kupffer Cells for Hepatitis B Virus Infection10:25

"Liver-on-a-Chip" Cultures of Primary Hepatocytes and Kupffer Cells for Hepatitis B Virus Infection

Published on: February 19, 2019

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...
Cytotoxic T Cells-mediated Immune Response01:27

Cytotoxic T Cells-mediated Immune Response

Cytotoxic T cells are a vital component of the immune system. They have the remarkable ability to identify and target antigens on infected or abnormal cells. These antigens often originate from intracellular pathogens such as viruses or abnormal proteins cancer cells produce.
Immunological surveillance is the ability of immune cells to monitor and eliminate infected cells with intracellular pathogens, neoplastically transformed cells, and cells with non-self antigens. Cytotoxic T cells and NK...
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...
Immune Response Against Viral Pathogens01:29

Immune Response Against Viral Pathogens

The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
NK Cells
NK cells are a crucial part of our innate immune system, acting as the first line of defense against viral infections. These cells can recognize and kill infected cells without prior exposure to the virus, effectively slowing down the spread of infection. Additionally, NK cells produce proinflammatory...
Inhibitors of Viral Protein Synthesis01:30

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...