Related Experiment Video

Updated: May 22, 2026

Long Term Intravital Multiphoton Microscopy Imaging of Immune Cells in Healthy and Diseased Liver Using CXCR6.Gfp Reporter Mice
11:44

Long Term Intravital Multiphoton Microscopy Imaging of Immune Cells in Healthy and Diseased Liver Using CXCR6.Gfp Reporter Mice

Published on: March 24, 2015

RANTES, TNF-α, oxidative stress, and hematological abnormalities in hepatitis C virus infection

Gamil Amin Tawadrous1, Amal A Aziz, Dalia G Amin

  • 1Department of Medical Biochemistry, Kasr Al-Aini Faculty of Medicine, Cairo University, Cairo, Egypt. gatawadrous@yahoo.com

Journal of Investigative Medicine : the Official Publication of the American Federation for Clinical Research
|April 27, 2012
PubMed

Insights

Hepatitis C virus (HCV) infection elevates inflammatory markers like RANTES and oxidative stress indicators (MDA, NO). These elevated levels correlate with viral load and may indicate liver injury, suggesting their use in monitoring HCV infection.

Area of Science:

  • Hepatology
  • Immunology
  • Virology

Background:

  • Chronic hepatitis C virus (HCV) infection impairs T-cell clearance and promotes B-cell abnormalities.
  • HCV infection induces systemic oxidative stress due to inflammation, iron overload, and liver damage.
  • Chemokines and their receptors are implicated in immune cell trafficking within the inflamed liver during viral infections.

Purpose of the Study:

  • To investigate the role of chemokines and oxidative stress markers in chronic HCV infection.
  • To assess the correlation between these markers and HCV viral load.
  • To evaluate potential monitoring markers for liver injury and oxidative stress in HCV patients.

Main Methods:

  • Study included 75 male subjects (30 controls, 45 HCV patients).
  • Assessed liver function tests, HCV RNA, RANTES, tumor necrosis factor alpha, malondialdehyde (MDA), and nitric oxide (NO).
  • HCV RNA viral load determined by real-time PCR; complete blood count analyzed.

Main Results:

  • HCV patients showed significantly higher levels of RANTES, tumor necrosis factor alpha, MDA, and NO compared to controls (P <0.05).
  • These markers positively correlated with HCV RNA viral load.
  • Patients exhibited mild leukopenia, thrombocytopenia, neutropenia, and lymphocytosis, increasing the lymphocytes/neutrophils ratio.

Conclusions:

  • Chemokines like RANTES are implicated as mediators of liver cell injury in HCV infection.
  • MDA and NO levels show potential as monitoring markers for oxidative stress in hepatitis C.
  • Findings support the use of these markers for assessing disease activity and liver damage in HCV.
Abstract

More Related Videos

A Cell Culture Model for Producing High Titer Hepatitis E Virus Stocks10:28

A Cell Culture Model for Producing High Titer Hepatitis E Virus Stocks

Published on: June 26, 2020

Induction of Drug-Induced, Autoimmune Hepatitis in BALB/c Mice for the Study of Its Pathogenic Mechanisms11:36

Induction of Drug-Induced, Autoimmune Hepatitis in BALB/c Mice for the Study of Its Pathogenic Mechanisms

Published on: May 29, 2020

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...
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...
Cirrhosis I: Introduction01:23

Cirrhosis I: Introduction

Cirrhosis is a chronic, irreversible liver disease characterized by the widespread replacement of healthy liver tissue with fibrotic scar tissue and the formation of regenerative nodules.Etiology of cirrhosisCirrhosis results from sustained liver injury that triggers progressive fibrosis and structural remodeling. The underlying causes are diverse, encompassing common and less frequent clinical conditions. Regardless of the origin, all causes lead to chronic inflammation, hepatocyte loss, and...
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 binding...
Hepatic Encephalopathy01:29

Hepatic Encephalopathy

DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...