title: Increased soluble IL-2 receptor levels during interferon and ribavirin treatment are associated with a good response in genotype 2a/2b patients with chronic hepatitis C.
abstract: OBJECTIVE
  Serum levels of soluble interleukin-2 receptor (sIL-2R) are known to serve as a marker for the activation of T lymphocytes. We measured serum levels of sIL-2R in patients with chronic hepatitis C (CHC) during interferon (IFN)-based treatment to determine the correlation between those levels and therapeutic efficacy, and to clarify whether there is a difference in the activation of T lymphocytes among HCV genotypes after the treatment.
  
  
  METHODS
  Forty-four patients received IFN-alpha2b monotherapy (group IFN-M), whereas 82 patients received the combination therapy with IFN-alpha2b and ribavirin (group IFN+R). We measured serum sIL-2R levels in these patients before (T0) and 2 weeks (T2) after the treatment.
  
  
  RESULTS
  The sustained virologic response rates in genotype 2a/2b patients were significantly higher than those in genotype 1b patients in both groups (P<0.005). In sustained virologic responders, sIL-2R levels at T2 were significantly higher than those at T0 in both groups (P<0.001). In nonresponders, sIL-2R levels at T2 were not different from those at T0 in group IFN-M, but were significantly higher than those at T0 in group IFN+R (P=0.0072). In genotype 1b patients, sIL-2R levels at T2 were not different from those at T0 in group IFN-M, but were significantly higher than those at T0 in group IFN+R (P=0.0064). In genotype 2a/2b patients, sIL-2R levels at T2 were significantly higher than those at T0 in both groups (P<0.0005).
  
  
  CONCLUSIONS
  These findings suggest that the activation of T lymphocytes after IFN-based treatment contributes to a high-sustained virologic response rate, especially in genotype 2a/2b patients.
authors.affiliation: Third Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan. s-abe@med.uoeh-u.ac.jp
authors.forename: Shintaro
authors.initials: S
authors.lastname: Abe
authors.forename: Ryoichi
authors.initials: R
authors.lastname: Narita
authors.forename: Toru
authors.initials: T
authors.lastname: Matsuhashi
authors.forename: Takeshi
authors.initials: T
authors.lastname: Oto
authors.forename: Akinari
authors.initials: A
authors.lastname: Tabaru
authors.forename: Makoto
authors.initials: M
authors.lastname: Otsuki
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000998:Antiviral Agents / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D004359:Drug Therapy, Combination; D005260:Female; D005838:Genotype; D016174:Hepacivirus / Q000235:genetics / Q000302:isolation & purification; D019698:Hepatitis C, Chronic / Q000188:drug therapy* / Q000276:immunology* / Q000821:virology; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000627:therapeutic use*; D008213:Lymphocyte Activation / Q000187:drug effects; D008297:Male; D008875:Middle Aged; D012367:RNA, Viral / Q000097:blood; D015375:Receptors, Interleukin-2 / Q000097:blood*; D011994:Recombinant Proteins; D012254:Ribavirin / Q000627:therapeutic use; D013601:T-Lymphocytes / Q000276:immunology; D016896:Treatment Outcome
chemical_list: D000998:Antiviral Agents; D015415:Biomarkers; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D012367:RNA, Viral; D015375:Receptors, Interleukin-2; D011994:Recombinant Proteins; D012254:Ribavirin