title: Cytokine and apoptosis gene polymorphisms influence the outcome of hepatitis C virus infection.
abstract: BACKGROUND
  Hepatitis C virus (HCV) infection is thought to be chronic and the factors leading to viral clearance or persistence are poorly understood. This study was undertaken to investigate the possibility of a significant relationship between the spontaneous clearance or the persistence of hepatitis C virus (HCV) infection and cytokine and apoptosis gene polymorphisms in Tunisian patients on hemodialysis.
  
  
  METHODS
  Polymorphisms of the genes IL-1 (-889 IL-1alpha, -511 and +3954 IL-1beta, IL-1Ra), IL-18 (-137 and -607), IL-12 (-1188) and Apo1/Fas (-670) were determined by PCR-RFLP, PCR-SSP and PCR-VNTR in 100 healthy blood donors and 100 patients infected with HCV and undergoing hemodialysis. The patients were classified into two groups: G1 consisted of 76 active chronic hepatitis patients (positive for HCV RNA) and G2 consisted of 24 hemodialysed patients who spontaneously eliminated the virus (negative for HCV RNA).
  
  
  RESULTS
  The frequency of genotype association [-137GC/-607CA] IL-18 was higher in G2 (41.7%) than in G1 (15.8%) (P=0.008; OR=0.26; 95% CI, 0.10-0.73). We also found a higher frequency of the AA genotype of the Apo1/Fas gene in G2 (41.6%) than in G1 (17.5%) (P=0.026; OR=3.49; 95% CI, 1.13-10.69). Adjustment for known covariate factors (age, gender and genotype) confirmed these univariate findings and revealed that the genotype association GC-CA of the (-137 and -607) IL-18 gene and the AA genotype of the Apo1/Fas gene were associated with the clearance of HCV (P=0.041 and 0.017, respectively).
  
  
  CONCLUSIONS
  The two genotypes GC-CA of the (-137 and -607) IL-18 polymorphism and the AA genotype of the Apo1/Fas gene influence the outcome of HCV infection in Tunisian patients on hemodialysis.
authors.affiliation: Immunology Research Laboratory of Kidney Transplantation and Immunopathology, Charles Nicolle Hospital, Thunis, Tunisia.
authors.forename: Leila
authors.initials: L
authors.lastname: Ksiaa Cheikhrouhou
authors.forename: Imen
authors.initials: I
authors.lastname: Sfar
authors.forename: Hajer
authors.initials: H
authors.lastname: Aounallah-Skhiri
authors.forename: Houda
authors.initials: H
authors.lastname: Aouadi
authors.forename: Salwa
authors.initials: S
authors.lastname: Jendoubi-Ayed
authors.forename: Taieb
authors.initials: T
authors.lastname: Ben Abdallah
authors.forename: Khaled
authors.initials: K
authors.lastname: Ayed
authors.forename: Yousr
authors.initials: Y
authors.lastname: Lakhoua-Gorgi
mesh_terms: D000328:Adult; D000368:Aged; D017209:Apoptosis / Q000235:genetics*; D016022:Case-Control Studies; D016009:Chi-Square Distribution; D016207:Cytokines / Q000235:genetics*; D005260:Female; D005787:Gene Frequency; D005838:Genotype; D016174:Hepacivirus / Q000235:genetics; D019698:Hepatitis C, Chronic / Q000175:diagnosis / Q000235:genetics* / Q000276:immunology / Q000473:pathology; D006801:Humans; D018664:Interleukin-12 / Q000235:genetics; D020382:Interleukin-18 / Q000235:genetics; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D010641:Phenotype; D011110:Polymorphism, Genetic; D011379:Prognosis; D012367:RNA, Viral / Q000097:blood; D006435:Renal Dialysis; D012189:Retrospective Studies; D013997:Time Factors; D014416:Tunisia; D019562:Viral Load; D019014:fas Receptor / Q000235:genetics*
chemical_list: D016207:Cytokines; C491901:FAS protein, human; D020382:Interleukin-18; D012367:RNA, Viral; D019014:fas Receptor; D018664:Interleukin-12