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Association of interleukin-18 polymorphisms and plasma level with the outcome of chronic HCV infection.
Bouzgarrou, N; Hassen, E; Schvoerer, E; Stoll-Keller, F; Bahri, O; Gabbouj, S; Cheikh, I; Maamouri, N; Mammi, N; Saffar, H; Trabelsi, A; Triki, H; Chouchane, L.
Afiliação
  • Bouzgarrou N; Laboratory of Molecular Immuno-oncology, Faculty of Medicine, Monastir, Tunisia. nadia.bouzgarrou@lycos.com
J Med Virol ; 80(4): 607-14, 2008 Apr.
Article em En | MEDLINE | ID: mdl-18297714
Hepatitis C virus (HCV) infection is the main cause of chronic liver disease throughout the world, and may progress to cirrhosis and hepatocellular carcinoma (HCC). Immunological factors, especially cytokines and some host genetic variations, rather than direct HCV action, seem to play an important role in the pathogenesis of HCV infection. Elevated levels of interleukin-18 (IL-18) were described previously for chronically (HCV)-infected patients. This study is aimed at investigating IL-18 promoter polymorphisms (-607C/A and -137G/C) in HCV-infected patients with different disease severities (chronic hepatitis C, liver cirrhosis and HCC) and establishing an association between these polymorphisms and IL-18 plasma concentration with the outcome of chronic HCV infection. The carriage of at least one C allele at position -607 (CC + CA) was associated with a higher risk of cirrhosis and HCC (P = 0.032). Compared with controls, HCV-infected patients had significantly higher levels of IL-18 (P = 0.0001) that correlate with disease severity (P = 0.01, P = 0.001, P = 0.0006, respectively). In conclusion, we supposed a possible implication of IL-18 promoter polymorphisms in the pathogenesis of chronic HCV infection.
Assuntos

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Polimorfismo Genético / Hepatite C Crônica / Interleucina-18 Idioma: En Ano de publicação: 2008 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Polimorfismo Genético / Hepatite C Crônica / Interleucina-18 Idioma: En Ano de publicação: 2008 Tipo de documento: Article