title: Neutralizing antibodies in patients with chronic hepatitis C infection treated with (Peg)-interferon/ribavirin.
abstract: BACKGROUND
  The role of neutralizing antibody (NAb) in determining response to antiviral therapy has not been established.
  
  
  OBJECTIVE
  In this study we have analysed the kinetic's of the NAb response in patients with chronic hepatitis C who received antiviral therapy.
  
  
  METHODS
  Seventeen patients infected with genotype 1, 2a/c or 3a hepatitis C virus (HCV) were enrolled, eight with a sustained virological response (SVR), five non-responders and four relapsers.
  
  
  RESULTS
  The mean NAb titre required to neutralize 50% of the E1E2-pp in patients who achieved an SVR (294+/-S.D. 51), in relapsers (246+/-S.D. 61.7) and non-responders (286+/-S.D. 80.95) did not differ significantly between the patient groups and did not alter during the course of treatment (P>0.01). Genetic variation present before antiviral therapy was analysed by single strand conformation polymorphism (SSCP) and failed to demonstrate a significant difference in the mean number of amplified E1E2 DNA fragments from the serum of patients who achieved an SVR (3.15+/-S.D. 1.53), relapsers (2.8+/-S.D. 1.32) or non-responders (3.69+/-S.D. 1.75). The baseline serum HCV viral loads were also not significantly different between patients who achieved an SVR (1.4 x 10(6) copies/ml; +/-S.D. 2.4 x 10(6)), relapsers (1.3 x 10(7) copies/ml; +/-S.D. 2.4 x 10(7)) and non-responders (1.5 x 10(6) copies/ml; +/-S.D. 1.1 x 10(6)).
  
  
  CONCLUSIONS
  We have shown that neutralizing anti-HCVpp antibody is not associated with response to antiviral therapy. In addition, there was no correlation between baseline virological load, circulating viral quasi-species, NAb titres and final response to treatment.
authors.affiliation: Macfarlane Burnet Institute for Medical Research and Public Health, Melbourne, Prahran, Victoria 3001, Australia.
authors.forename: Irene
authors.initials: I
authors.lastname: Boo
authors.forename: Alexandra E
authors.initials: AE
authors.lastname: Fischer
authors.forename: Doug
authors.initials: D
authors.lastname: Johnson
authors.forename: Ruth
authors.initials: R
authors.lastname: Chin
authors.forename: Maxine
authors.initials: M
authors.lastname: Giourouki
authors.forename: Mandvi
authors.initials: M
authors.lastname: Bharadwaj
authors.forename: Scott
authors.initials: S
authors.lastname: Bowden
authors.forename: Joseph
authors.initials: J
authors.lastname: Torresi
authors.forename: Heidi
authors.initials: H
authors.lastname: Drummer
mesh_terms: D000998:Antiviral Agents / Q000627:therapeutic use*; D004359:Drug Therapy, Combination; D016174:Hepacivirus / Q000145:classification / Q000187:drug effects / Q000235:genetics / Q000276:immunology*; D018937:Hepatitis C Antibodies / Q000097:blood / Q000276:immunology*; D019698:Hepatitis C, Chronic / Q000188:drug therapy* / Q000276:immunology* / Q000821:virology; D006801:Humans; D007372:Interferons / Q000627:therapeutic use; D009500:Neutralization Tests; D011092:Polyethylene Glycols / Q000627:therapeutic use; D018807:Polymorphism, Single-Stranded Conformational; D012254:Ribavirin / Q000627:therapeutic use; D014759:Viral Envelope Proteins / Q000276:immunology
chemical_list: D000998:Antiviral Agents; C087035:E1 protein, Hepatitis C virus; D018937:Hepatitis C Antibodies; D014759:Viral Envelope Proteins; C091015:glycoprotein E2, Hepatitis C virus; D011092:Polyethylene Glycols; D012254:Ribavirin; D007372:Interferons