title: Influence of viral genotype and level of viremia on the severity of liver injury and the response to interferon therapy in Spanish patients with chronic C infection.
abstract: BACKGROUND
  We wanted to investigate the influence of viral genotype on the severity of liver injury and response to interferon and whether the level of viremia differs in accordance with genotype, severity of liver disease, and response to interferon in patients with hepatitis C virus (HCV) infection.
  
  
  METHODS
  We studied 118 patients with HCV-related liver disease. HCV genotypes were determined with a line probe assay, and serum HCV RNA levels with a competitive reverse transcription polymerase chain reaction assay.
  
  
  RESULTS
  HCV type 1b was the most prevalent genotype (88%). It was present in 100% of cirrhotic patients, with or without hepatocellular carcinoma (HCC), but only in 78% of patients with chronic hepatitis (P < 0.001). The response to interferon was better in patients infected with non-1b HCV genotypes (P = 0.002). In a multivariate analysis non-1b HCV genotypes and a low hepatic fibrosis correlated with a favorable response to interferon. Among patients with chronic hepatitis those infected with HCV type 1b were older (P < 0.001), and age was the only independent factor associated with HCV type 1b. Viremia levels differed neither between genotypes nor in response to interferon and was significantly lower in patients with cirrhosis and HCC.
  
  
  CONCLUSIONS
  HCV 1b was associated with more severe liver disease and a worse response to interferon therapy. Non-1b genotypes and a lower liver fibrosis were the only independent predictors of a favorable response to interferon. Levels of HCV viremia differed neither among different genotypes nor in response to interferon and decreased with advanced liver disease.
authors.affiliation: Dept. of Gastroenterology, Doce de Octubre Hospital, Madrid, Spain.
authors.forename: I
authors.initials: I
authors.lastname: Fernández
authors.forename: G
authors.initials: G
authors.lastname: Castellano
authors.forename: M J
authors.initials: MJ
authors.lastname: Domingo
authors.forename: A
authors.initials: A
authors.lastname: Fuertes
authors.forename: F
authors.initials: F
authors.lastname: Colina
authors.forename: F
authors.initials: F
authors.lastname: Canga
authors.forename: F J
authors.initials: FJ
authors.lastname: de la Cruz
authors.forename: A G
authors.initials: AG
authors.lastname: de la Cámara
authors.forename: J A
authors.initials: JA
authors.lastname: Solís
mesh_terms: D000368:Aged; D000998:Antiviral Agents / Q000627:therapeutic use*; D005260:Female; D005838:Genotype; D016174:Hepacivirus / Q000235:genetics* / Q000502:physiology; D006526:Hepatitis C / Q000188:drug therapy* / Q000473:pathology / Q000821:virology*; D006801:Humans; D016898:Interferon-alpha / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D011446:Prospective Studies; D012367:RNA, Viral / Q000097:blood; D014766:Viremia / Q000188:drug therapy* / Q000235:genetics* / Q000473:pathology; D014779:Virus Replication
chemical_list: D000998:Antiviral Agents; D016898:Interferon-alpha; D012367:RNA, Viral