title: Altered of apoptotic markers of both extrinsic and intrinsic pathways induced by hepatitis C virus infection in peripheral blood mononuclear cells.
abstract: BACKGROUND
  Chronic hepatitis C (CHC) has emerged as a leading cause of cirrhosis in the U.S. and across the world. To understand the role of apoptotic pathways in hepatitis C virus (HCV) infection, we studied the mRNA and protein expression patterns of apoptosis-related genes in peripheral blood mononuclear cells (PBMC) obtained from patients with HCV infection.
  
  
  METHODS
  The present study included 50 subjects which plasma samples were positive for HCV, but negative for human immunodeficiency virus (HIV) or hepatitis B virus (HBV). These cases were divided into four groups according to METAVIR, a score-based analysis which helps to interpret a liver biopsy according to the degree of inflammation and fibrosis. mRNA expression of the studied genes were analyzed by reverse transcription of quantitative polymerase chain reaction (RT-qPCR) and protein levels, analyzed by ELISA, was also conducted. HCV genotyping was also determined.
  
  
  RESULTS
  HCV infection increased mRNA expression and protein synthesis of caspase 8 in group 1 by 3 fold and 4 fold, respectively (p < 0.05). In group 4 HCV infection increased mRNA expression and protein synthesis of caspase 9 by 2 fold and 1,5 fold, respectively (p < 0.05). Also, caspase 3 mRNA expression and protein synthesis had level augumented by HCV infection in group 1 by 4 fold and 5 fold, respectively, and in group 4 by 6 fold and 7 fold, respectively (p < 0.05).
  
  
  CONCLUSIONS
  HCV induces alteration at both genomic and protein levels of apoptosis markers involved with extrinsic and intrinsic pathways.
authors.affiliation: Colsan - Associação Beneficente de Coleta de Sangue, São Paulo, SP, Brazil. albertonig@nefro.epm.br
authors.forename: Guilherme
authors.initials: G
authors.lastname: Albertoni
authors.forename: Carine Prisco
authors.initials: CP
authors.lastname: Arnoni
authors.forename: Flávia Roche Moreira
authors.initials: FR
authors.lastname: Latini
authors.forename: Sheila Siqueira
authors.initials: SS
authors.lastname: Andrade
authors.forename: Patrícia Regina Barboza
authors.initials: PR
authors.lastname: Araújo
authors.forename: Flaviane Kesia
authors.initials: FK
authors.lastname: Rodrigues
authors.forename: Patrícia Bortman
authors.initials: PB
authors.lastname: Rozenchan
authors.forename: Maria Cássia
authors.initials: MC
authors.lastname: Mendes-Correa
authors.forename: Olavo Henrique Munhoz
authors.initials: OH
authors.lastname: Leite
authors.forename: Nestor
authors.initials: N
authors.lastname: Schor
authors.forename: Manoel João Castelo Batista
authors.initials: MJ
authors.lastname: Girão
authors.forename: José Augusto
authors.initials: JA
authors.lastname: Barreto
mesh_terms: D000328:Adult; D017209:Apoptosis; D015415:Biomarkers / Q000097:blood; D015153:Blotting, Western; D053148:Caspase 3 / Q000096:biosynthesis; D053181:Caspase 8 / Q000096:biosynthesis; D053453:Caspase 9 / Q000096:biosynthesis; D005260:Female; D020869:Gene Expression Profiling; D005838:Genotype; D016174:Hepacivirus / Q000145:classification / Q000235:genetics; D019698:Hepatitis C, Chronic / Q000150:complications / Q000276:immunology* / Q000473:pathology* / Q000821:virology; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000276:immunology* / Q000821:virology*; D008099:Liver / Q000473:pathology; D008103:Liver Cirrhosis / Q000209:etiology / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D060888:Real-Time Polymerase Chain Reaction; D012720:Severity of Illness Index
chemical_list: D015415:Biomarkers; D053148:Caspase 3; D053181:Caspase 8; D053453:Caspase 9