title: Hepatitis C virus genotypes and hepatic fibrosis regulate 24-h decline of serum hepatitis C virus RNA during interferon therapy in patients with chronic hepatitis C.
abstract: OBJECTIVE
  Recently, hepatitis C virus (HCV) dynamics during interferon (IFN) therapy have been studied in detail. We examined factors that regulate the viral kinetics and the relationship between the viral kinetics and clinical effect of IFN therapy.
  
  
  METHODS
  Eighty-eight patients with chronic hepatitis C entered this study. All patients had been treated with 3 MU of IFN-beta twice a day for the first 2-4 weeks, then IFN-alpha for the next 20-22 weeks (three injections per week). The levels of serum HCV RNA were determined by Amplicor HCV Monitor version 1.0, before and 24 h after the first injection of IFN; then the decline of HCV was calculated. Liver inflammation and fibrosis were scored as 0 (none), 1 (mild), 2 (moderate) or 3 (severe) using biopsy specimens.
  
  
  RESULTS
  The decline of serum HCV RNA was 1.42 +/- 0.65 log copies/mL in genotype 1b and 1.83 +/- 0.72 in genotype 2a or 2b (P < 0.01). By a logistic regression model, genotype (1b, 2a or 2b) and hepatic fibrosis (0 or 1, 2 or 3) associated with 24-h decline of serum HCV RNA, independently. As the predictor of IFN therapy, the decline of serum HCV RNA and serum HCV RNA levels before IFN therapy were the independent significant factors (P < 0.001).
  
  
  CONCLUSIONS
  The decline of serum HCV RNA during the first 24 h of IFN therapy was regulated by genotypes and hepatic fibrosis. The decline of serum HCV RNA and initial HCV load were independent factors that can be the predictor of the subsequent sustained viral response to IFN therapy.
authors.affiliation: Departments of Hepatology, Sapporo Kosei General Hospital, Sapporo, Japan. ykarino@jcom.home.ne.jp
authors.forename: Yoshiyasu
authors.initials: Y
authors.lastname: Karino
authors.forename: Jouji
authors.initials: J
authors.lastname: Toyota
authors.forename: Masaaki
authors.initials: M
authors.lastname: Sugawara
authors.forename: Kayo
authors.initials: K
authors.lastname: Miyazaki
authors.forename: Yasuaki
authors.initials: Y
authors.lastname: Kuwata
authors.forename: Katsu
authors.initials: K
authors.lastname: Yamazaki
authors.forename: Takahiro
authors.initials: T
authors.lastname: Sato
authors.forename: Takumi
authors.initials: T
authors.lastname: Ohmura
authors.forename: Takashi
authors.initials: T
authors.lastname: Matsushima
mesh_terms: D000328:Adult; D000368:Aged; D000998:Antiviral Agents / Q000627:therapeutic use*; D005260:Female; D005838:Genotype; D016174:Hepacivirus / Q000187:drug effects / Q000235:genetics* / Q000302:isolation & purification*; D019698:Hepatitis C, Chronic / Q000097:blood* / Q000188:drug therapy / Q000235:genetics*; D006801:Humans; D016898:Interferon-alpha / Q000627:therapeutic use*; D016899:Interferon-beta / Q000627:therapeutic use*; D008103:Liver Cirrhosis / Q000097:blood* / Q000188:drug therapy / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D017063:Outcome Assessment, Health Care; D011237:Predictive Value of Tests; D012313:RNA / Q000097:blood* / Q000187:drug effects / Q000235:genetics*; D012720:Severity of Illness Index; D013997:Time Factors; D019562:Viral Load
chemical_list: D000998:Antiviral Agents; D016898:Interferon-alpha; D012313:RNA; D016899:Interferon-beta