Related Experiment Video

Updated: Apr 27, 2026

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

11.2K

Inhibition of c3 convertase activity by hepatitis C virus as an additional lesion in the regulation of complement

Hangeun Kim1, Keith Meyer1, Adrian M Di Bisceglie2

  • 1Department of Internal Medicine, Saint Louis University, St. Louis, Missouri, United States of America.

Plos One
|July 2, 2014
PubMed

Insights

Hepatitis C virus (HCV) infection weakens the innate immune system by inhibiting complement component 2 (C2) and Factor I. This impairs the complement system

Area of Science:

  • Immunology
  • Virology
  • Hepatology

Background:

  • Hepatitis C virus (HCV) infection is known to attenuate the complement system at multiple levels.
  • Previous studies indicated that complement system attenuation occurs in chronically HCV-infected livers, regardless of disease stage.
  • Complete impairment of complement pathways was not observed through single regulatory mechanisms.

Purpose of the Study:

  • To investigate the regulation of complement component 2 (C2) expression in hepatoma cells infected with HCV in vitro.
  • To validate findings in liver biopsy specimens from chronically HCV-infected patients.
  • To elucidate the role of C2 and Factor I in HCV-induced complement system modulation.

Main Methods:

  • In vitro infection of hepatoma cells with cell culture-grown HCV.
  • Analysis of C2 mRNA expression levels.
  • Assessment of classical C3 convertase (C4b2a) activity.
  • Measurement of C3b deposition on bacterial membranes using patient sera.
  • Quantification of iC3b levels in patient sera.
  • Evaluation of Factor I and Factor H expression in liver biopsy specimens.

Main Results:

  • HCV infection significantly inhibited C2 mRNA expression in hepatoma cells.
  • Classical C3 convertase activity (C4b2a) was decreased in infected cells.
  • Reduced C3b deposition and lower iC3b levels in HCV-infected patient sera indicated impaired C3 convertase and Factor I activity.
  • Factor I expression was significantly reduced in HCV-infected liver biopsies, while Factor H remained unchanged or increased.

Conclusions:

  • HCV infection leads to significant inhibition of C2 expression and C3 convertase activity.
  • Impairment of Factor I activity is another mechanism employed by HCV to weaken the complement system.
  • These combined effects contribute to the overall attenuation of the complement system, weakening the innate immune response against HCV.

More Related Videos

A Protocol for Analyzing Hepatitis C Virus Replication13:04

A Protocol for Analyzing Hepatitis C Virus Replication

Published on: June 26, 2014

23.7K
A Competent Hepatocyte Model Examining Hepatitis B Virus Entry through Sodium Taurocholate Cotransporting Polypeptide as a Therapeutic Target11:34

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

Published on: May 10, 2022

2.2K

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.
80
Complement System01:27

Complement System

The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a...
10.5K
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...
57
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...
21
Effect of Hepatic Disease on Pharmacokinetics: Drug Dosing and Hepatic Blood Flow01:26

Effect of Hepatic Disease on Pharmacokinetics: Drug Dosing and Hepatic Blood Flow

Chronic liver disease significantly impacts drug metabolism due to alterations in hepatic blood flow and enzyme accessibility. This disruption affects the body's pharmacokinetics—the movement and processing of drugs within the system. Key enzymes crucial for metabolizing medications become less accessible, changing how drugs are processed and utilized. Furthermore, liver disease influences the synthesis of plasma proteins, such as albumin and globulins, which play critical roles in drug...
380
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...
34