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HCV-MEDIATED APOPTOSIS OF HEPATOCYTES IN CULTURE AND VIRAL PATHOGENESIS.
Gene expression
Cell staining
DNA-binding proteins
Flow cytometry
Proteases
Hepatitis C virus
Necrosis
Autor
Afiliación
Office of Blood Research and Review. Division of Emerging Transfusion Transmitted Diseases. Laboratory of Emerging Pathogens. Silver Spring, MD, United States of America
Office of Blood Research and Review. Division of Emerging Transfusion Transmitted Diseases. Laboratory of Emerging Pathogens. Silver Spring, MD, United States of America
Federal University of Mato Grosso do Sul. Campo Grande, MT, Brazil/ Office of Blood Research and Review. Division of Emerging Transfusion Transmitted Diseases. Laboratory of Emerging Pathogens. Silver Spring, MD, United States of America
Office of Blood Research and Review. Division of Emerging Transfusion Transmitted Diseases. Laboratory of Emerging Pathogens. Silver Spring, MD, United States of America
Fundação Oswaldo Cruz. Centro de Pesquisas René Rachou. Grupo Integrado de Pesquisas em Biomarcadores. Belo Horizonte, MG, Brazil/Office of Blood Research and Review. Division of Emerging Transfusion Transmitted Diseases. Laboratory of Emerging Pathogens. Silver Spring, MD, United States of America
Universite Francois Rabelais and CHRU de Tours. Tours, France
Office of Blood Research and Review. Division of Emerging Transfusion Transmitted Diseases. Laboratory of Emerging Pathogens. Silver Spring, MD, United States of America
Office of Blood Research and Review. Division of Emerging Transfusion Transmitted Diseases. Laboratory of Emerging Pathogens. Silver Spring, MD, United States of America
Federal University of Mato Grosso do Sul. Campo Grande, MT, Brazil/ Office of Blood Research and Review. Division of Emerging Transfusion Transmitted Diseases. Laboratory of Emerging Pathogens. Silver Spring, MD, United States of America
Office of Blood Research and Review. Division of Emerging Transfusion Transmitted Diseases. Laboratory of Emerging Pathogens. Silver Spring, MD, United States of America
Fundação Oswaldo Cruz. Centro de Pesquisas René Rachou. Grupo Integrado de Pesquisas em Biomarcadores. Belo Horizonte, MG, Brazil/Office of Blood Research and Review. Division of Emerging Transfusion Transmitted Diseases. Laboratory of Emerging Pathogens. Silver Spring, MD, United States of America
Universite Francois Rabelais and CHRU de Tours. Tours, France
Office of Blood Research and Review. Division of Emerging Transfusion Transmitted Diseases. Laboratory of Emerging Pathogens. Silver Spring, MD, United States of America
Resumen en ingles
Chronic Hepatitis C Virus (HCV) infection is associated with progressive liver injury and subsequent development of fibrosis and cirrhosis. The death of hepatocytes results in the release of cytokines that induce inflammatory and fibrotic responses. The mechanism of liver damage is still under investigation but both apoptosis and immune-mediated processes may play roles. By observing the changes in gene expression patterns in HCV-infected cells, both markers and the causes of HCV-associated liver injury may be elucidated. HCV genotype 1b virus from persistently infected VeroE6 cells induced a strong cytopathic effect when used to infect Huh7.5 hepatoma cells. To determine if this cytopathic effect was a result of apoptosis, ultrastructural changes were observed by electron microscopy and markers of programmed cell death were surveyed. Screening of a human PCR array demonstrated a gene expression profile that contained upregulated markers of apoptosis, including tumor necrosis factor, caspases and caspase activators, Fas, Bcl2-interacting killer (BIK) and tumor suppressor protein, p53, as a result of HCV genotype 1b infection. The genes identified in this study should provide new insights into understanding viral pathogenesis in liver cells and may possibly help to identify novel antiviral and antifibrotic targets.
Palabras clave en portugues
ApoptosisPalabras clave en ingles
ApoptosisGene expression
Cell staining
DNA-binding proteins
Flow cytometry
Proteases
Hepatitis C virus
Necrosis
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