Mechanisms of Liver Injury. III. Oxidative stress in the pathogenesis of hepatitis C virus

2006 ◽  
Vol 290 (5) ◽  
pp. G847-G851 ◽  
Author(s):  
Jinah Choi ◽  
J.-H. James Ou
Keyword(s):  
Oxidative Stress ◽  
Hepatocellular Carcinoma ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Liver Injury ◽  
Iron Overload ◽  
Antioxidant Defense ◽  
Hcv Infection ◽  
Nitrogen Species ◽  
Systemic Oxidative Stress

Hepatitis C virus (HCV) is a major cause of viral hepatitis that can progress to hepatic fibrosis, steatosis, hepatocellular carcinoma, and liver failure. HCV infection is characterized by a systemic oxidative stress that is most likely caused by a combination of chronic inflammation, iron overload, liver damage, and proteins encoded by HCV. The increased generation of reactive oxygen and nitrogen species, together with the decreased antioxidant defense, promotes the development and progression of hepatic and extrahepatic complications of HCV infection. This review discusses the possible mechanisms of HCV-induced oxidative stress and its role in HCV pathogenesis.

scholarly journals Association of Hepatocellular Carcinoma (HCC) With Hepatitis B Virus (HBV) Versus Hepatitis C Virus (HCV) Infection Among Different Asian Subgroups

2011 ◽  
Vol 140 (5) ◽  
pp. S-924-S-925 ◽  
Author(s):  
Hillary Lin ◽  
Nghiem B. Ha ◽  
Deawodi Ladzekpo ◽  
Aijaz Ahmed ◽  
Walid Ayoub ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Hcv Infection ◽  
B Virus

scholarly journals PATHOPHYSIOLOGIC MECHANISMS OF THE INFLUENCE OF TISSUE RESPIRATION ENZYMES ON THE MITOCHONDRIAL FUNCTION IN PATIENTS WITH CHRONIC HEPATITIS C

2018 ◽  
Vol 22 (1-2) ◽  
pp. 7-10
Author(s):  
I.Y. Bagmut ◽  
S.M. Gramatiuk
Keyword(s):  
Oxidative Stress ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Cytochrome C ◽  
Hcv Infection ◽  
Tissue Respiration ◽  
Pathophysiological Mechanism ◽  
Mitochondrial Division ◽  
Isolated Mitochondria ◽  
Viral Hepatitis C

Studies conducted over several decades in the field of pathophysiological mechanisms of hepatocyte mitochondria have usually been directed to functional studies of isolated mitochondria in the absence of ADP. In many cases, researchers used data to calculate parameters, including the respiratory rate or the amount of ADP consumed for each amount of oxygen used. However, so far, little is known about how the virus can survive in a highly oxidizing environment, given that oxidative stress is such an outstanding clinical feature that is associated with infection with the hepatitis C virus. In our opinion, adaptation to oxidative stress is a pathophysiological mechanism for the survival of the virus. The objective is to research mechanisms of energy supply disturbance as a mechanism of damage to cells in patients with chronic viral hepatitis C. The 62 HCV+ patients and 24 healthy controls were enrolled in the present cross-sectional study.  The patients were selected on the basis of their stable clinical condition over the past 3 months. The HCV infection was diagnosed by the positivity of anti-HCV and HCV-RNA for at least 6 months of period. Mitochondrial integrity was assessed by cytochrome C release using a commercial kit (Cytochrome C Oxidase Assay Kit, Sigma-Aldrich, St. Louis) indicating a mean of 96% intact mitochondria. Intrinsic NADH fluorescence was monitored in isolated mitochondria as a marker of the mitochondrial NADH redox state. Mitochondrial division is a key determinant of mitochondrial quality control, and HCV modulates these key processes in the adaptation to cellular physiological perturbations associated with infection to promote viral persistence. Mitochondrial division is not invariably associated with cell death but can also protect cells from death induced by oxidative stress and Ca2+-dependent apoptotic stimuli. The mechanism by which enzymes for energy metabolism suppress the replication of the hepatitis C virus is not yet clear, but it probably includes calcium and dissociation of the mammalian replication complex. A detailed understanding of the mechanism by which energy enzymes suppress the replication of HCV infection require additional research.

scholarly journals Role of hepatitis C virus(HCV) infection on liver injury in Sjoegren's syndrome(Sjs).

Kanzo ◽  
1994 ◽  
Vol 35 (11) ◽  
pp. 783-790 ◽  
Author(s):  
Hideyuki KOJIMA ◽  
Keiji KITAGAMI ◽  
Masahito UEMURA ◽  
Yoshinobu MATSUMURA ◽  
Motoyuki YOSHIDA ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Liver Injury ◽  
Hcv Infection ◽  
Sjoegren’S Syndrome

scholarly journals Successful Treatment of Oral Lichen Planus with Direct-Acting Antiviral Agents after Liver Transplantation for Hepatitis C Virus-Associated Hepatocellular Carcinoma

2017 ◽  
Vol 11 (3) ◽  
pp. 701-710 ◽  
Author(s):  
Yumiko Nagao ◽  
Kazunori Nakasone ◽  
Tatsuji Maeshiro ◽  
Nao Nishida ◽  
Kanae Kimura ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Transplantation ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Lichen Planus ◽  
Oral Lichen Planus ◽  
Immunosuppressive Drugs ◽  
Hcv Infection ◽  
Direct Acting ◽  
Oral Lichen

Hepatitis C virus (HCV) infection is frequently associated with various extrahepatic manifestations, such as autoimmune features and immune complex deposit diseases. Oral lichen planus (OLP) is one such extrahepatic manifestation of HCV infection. Recently, direct-acting antivirals (DAA) have proved to be highly effective and safe for the eradication of HCV. Herein, we report a case of OLP accompanied by HCV-related hepatocellular carcinoma (HCC) that disappeared after liver transplantation and achievement of sustained virological response following interferon (IFN)-free treatment with ledipasvir (LDV) and sofosbuvir (SOF). The 50-year-old patient developed erosive OLP during IFN therapy, with hyperthyroidism at 53 years of age and HCC at 55 years. He received immunosuppressive drugs and IFN-free DAA treatment after liver transplantation at 60 years of age, which led to disappearance of the symptoms of OLP. The patient was treated safely and effectively with LDV/SOF, although it is not known whether the disappearance of OLP resulted from the eradication of HCV or the immunosuppressive therapy.

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