Role of matrix metalloproteinases, proinflammatory cytokines, and oxidative stress–derived molecules in hepatitis C virus–associated mixed cryoglobulinemia vasculitis neuropathy

2007 ◽  
Vol 56 (4) ◽  
pp. 1315-1324 ◽  
Author(s):  
David Saadoun ◽  
Ivan Bieche ◽  
François-Jérome Authier ◽  
Ingrid Laurendeau ◽  
Florence Jambou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Matrix Metalloproteinases ◽  
Proinflammatory Cytokines ◽  
Mixed Cryoglobulinemia ◽  
And Oxidative Stress

Protective role of amantadine in mitochondrial dysfunction and oxidative stress mediated by hepatitis C virus protein expression

2014 ◽  
Vol 89 (4) ◽  
pp. 545-556 ◽  
Author(s):  
Giovanni Quarato ◽  
Rosella Scrima ◽  
Maria Ripoli ◽  
Francesca Agriesti ◽  
Darius Moradpour ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Protein Expression ◽  
Mitochondrial Dysfunction ◽  
Protective Role ◽  
Virus Protein ◽  
And Oxidative Stress

scholarly journals Immunválasz és oxidatív stressz hepatitis C-vírus-infekcióban

2015 ◽  
Vol 156 (47) ◽  
pp. 1898-1903
Author(s):  
Alajos Pár ◽  
Gabriella Pár
Keyword(s):  
Oxidative Stress ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Immune Responses ◽  
Current Knowledge ◽  
Oxygen Species ◽  
Adaptive Immune Responses ◽  
Adaptive Immune ◽  
And Oxidative Stress

This review summarizes our current knowledge on the innate and adaptive immune responses induced by hepatitis C virus, and on the genetic polymorphisms that may determine the outcome of the disease. In addition, the authors discuss the role of reactive oxygen species and oxidative stress in hepatitis C virus-related pathogenic processess, such as hepatitis, fibrosis, hepatocellular carcinoma, steatosis and insulin resistance. Orv. Hetil., 2015, 156(47), 1898–1903.

scholarly journals Branched‐chain amino acids reduce hepatic iron accumulation and oxidative stress in hepatitis C virus polyprotein‐expressing mice

2014 ◽  
Vol 35 (4) ◽  
pp. 1303-1314 ◽  
Author(s):  
Masaaki Korenaga ◽  
Sohji Nishina ◽  
Keiko Korenaga ◽  
Yasuyuki Tomiyama ◽  
Naoko Yoshioka ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Amino Acids ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Branched Chain Amino Acids ◽  
Iron Accumulation ◽  
Hepatic Iron ◽  
Branched Chain ◽  
Virus Polyprotein ◽  
And Oxidative Stress

[433] FK506 AMELIORATES METABOLIC DISTURBANCE AND OXIDATIVE STRESS IN HEPATITIS C VIRUS INFECTION

2007 ◽  
Vol 46 ◽  
pp. S165-S166
Author(s):  
K. Moriya ◽  
H. Miyoshi ◽  
S. Shinzawa ◽  
T. Tsutsumi ◽  
H. Fujie ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Virus Infection ◽  
Metabolic Disturbance ◽  
Hepatitis C Virus Infection ◽  
And Oxidative Stress

scholarly journals Hepatitis C Virus (HCV) Constitutively Activates STAT-3 via Oxidative Stress: Role of STAT-3 in HCV Replication

2005 ◽  
Vol 79 (3) ◽  
pp. 1569-1580 ◽  
Author(s):  
Gulam Waris ◽  
James Turkson ◽  
Tarek Hassanein ◽  
Aleem Siddiqui
Keyword(s):  
Oxidative Stress ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Dominant Negative ◽  
Mitogen Activated Protein Kinase ◽  
Hcv Rna ◽  
Pyrrolidine Dithiocarbamate ◽  
Constitutive Activation ◽  
Mitogen Activated Protein

ABSTRACT The hepatitis C virus (HCV) causes chronic hepatitis, which often results in liver cirrhosis and hepatocellular carcinoma. We have previously shown that HCV nonstructural proteins induce activation of STAT-3 via oxidative stress and Ca2+ signaling (G. Gong, G. Waris, R. Tanveer, and A. Siddiqui, Proc. Natl. Acad. Sci. USA 98:9599-9604, 2001). In this study, we focus on the signaling pathway leading to STAT-3 activation in response to oxidative stress induced by HCV translation and replication activities. Here, we demonstrate the constitutive activation of STAT-3 in HCV replicon-expressing cells. The HCV-induced STAT-3 activation was inhibited in the presence of antioxidant (pyrrolidine dithiocarbamate) and Ca2+ chelators (BAPTA-AM and TMB-8). Previous studies have shown that maximum STAT-3 transactivation requires Ser727 phosphorylation in addition to tyrosine phosphorylation. Using a series of inhibitors and dominant negative mutants, we show that HCV-induced activation of STAT-3 is mediated by oxidative stress and influenced by the activation of cellular kinases, including p38 mitogen-activated protein kinase, JNK, JAK-2, and Src. Our results also suggest a potential role of STAT-3 in HCV RNA replication. We also observed the constitutive activation of STAT-3 in the liver biopsy of an HCV-infected patient. These studies provide an insight into the mechanisms by which HCV induces intracellular events relevant to liver pathogenesis associated with the viral infection.

scholarly journals Genetic determinants in hepatitis C virus-associated mixed cryoglobulinemia: Role of polymorphic variants of BAFF promoter and Fcγ receptors

2011 ◽  
Vol 63 (5) ◽  
pp. 1446-1451 ◽  
Author(s):  
Laura Gragnani ◽  
Alessia Piluso ◽  
Carlo Giannini ◽  
Patrizio Caini ◽  
Elisa Fognani ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Mixed Cryoglobulinemia ◽  
Genetic Determinants ◽  
Fcγ Receptors ◽  
Polymorphic Variants

scholarly journals Arsenic Trioxide Inhibits Hepatitis C Virus RNA Replication through Modulation of the Glutathione Redox System and Oxidative Stress

2008 ◽  
Vol 83 (5) ◽  
pp. 2338-2348 ◽  
Author(s):  
Misao Kuroki ◽  
Yasuo Ariumi ◽  
Masanori Ikeda ◽  
Hiromichi Dansako ◽  
Takaji Wakita ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Arsenic Trioxide ◽  
Redox System ◽  
Rna Replication ◽  
Hcv Rna ◽  
Glutathione Redox System ◽  
And Oxidative Stress ◽  
Glutathione Redox

ABSTRACT Arsenic trioxide (ATO), a therapeutic reagent used for the treatment of acute promyelocytic leukemia, has recently been reported to increase human immunodeficiency virus type 1 infectivity. However, in this study, we have demonstrated that replication of genome-length hepatitis C virus (HCV) RNA (O strain of genotype 1b) was notably inhibited by ATO at submicromolar concentrations without cell toxicity. RNA replication of HCV-JFH1 (genotype 2a) and the release of core protein into the culture supernatants were also inhibited by ATO after the HCV infection. To clarify the mechanism of the anti-HCV activity of ATO, we examined whether or not PML is associated with this anti-HCV activity, since PML is known to be a target of ATO. Interestingly, we observed the cytoplasmic translocation of PML after treatment with ATO. However, ATO still inhibited the HCV RNA replication even in the PML knockdown cells, suggesting that PML is dispensable for the anti-HCV activity of ATO. In contrast, we found that N-acetyl-cysteine, an antioxidant and glutathione precursor, completely and partially eliminated the anti-HCV activity of ATO after 24 h and 72 h of treatment, respectively. In this context, it is worth noting that we found an elevation of intracellular superoxide anion radical, but not hydrogen peroxide, and the depletion of intracellular glutathione in the ATO-treated cells. Taken together, these findings suggest that ATO inhibits the HCV RNA replication through modulation of the glutathione redox system and oxidative stress.

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