title: HCV antibody quantitative levels in liver transplant patients: do they have any relevance in clinical practice?
abstract: OBJECTIVE
  Hepatitis C virus (HCV) is not directly cytopathic to the hepatocytes; however, host immune response against the virus does cause hepatic injury. Production of the HCV antibody is a host immune response to a viral antigen. The currently used HCV antibody assay is a qualitative, not quantitative, assessment. In this study, we sought to quantitatively estimate HCV antibody levels in patients who had undergone liver transplantations at the University of Rochester Medical Center, Rochester, New York, and correlate these levels with HCV RNA viral load, genotype, severity of recurrence, and anti-HCV treatment.
  
  
  METHODS
  From 39 liver transplantation patients, we obtained 141 blood samples for quantitative HCV RNA to measure HCV antibody levels quantitatively.
  
  
  RESULTS
  Most antibody levels were within a narrow range with a mean of 32.9+/-5.1. Samples with undetectable RNA had a mean antibody level of 31.4+/-8.0, and samples with a positive RNA had mean level of 33.0+/-4.6. The mean antibody levels were significantly higher for patients with genotype 1 (n=33) compared with those with genotype 2 (n=5) (33.2 vs 29.1; P=.007). No correlation was found between antibody levels and severity of hepatic injury with regard to hepatitis activity index or fibrosis score. Six patients with no response to anti-HCV treatment had no change in their mean antibody levels (33.7 vs 34.5). Ten patients who responded to anti-HCV therapy had lower mean levels after therapy, but the changes were not significant (34.2 vs 30.4).
  
  
  CONCLUSIONS
  Antibody levels in this study did not correlate with viral load or hepatic injury. However, genotype-2 patients had significantly lower levels compared with genotype-1 patients, and patients who responded to anti-HCV therapy demonstrated decreased antibody levels.
authors.affiliation: University of Rochester Medical Center, Division of Transplantation, Department of Surgery, Rochester, NY 14642, USA. ashok_jain@urmc.rochester.edu
authors.forename: Ashok
authors.initials: A
authors.lastname: Jain
authors.forename: Marilyn
authors.initials: M
authors.lastname: Menegus
authors.forename: Ravi
authors.initials: R
authors.lastname: Mohanka
authors.forename: Mark
authors.initials: M
authors.lastname: Orloff
authors.forename: Peter
authors.initials: P
authors.lastname: Abt
authors.forename: Parvez
authors.initials: P
authors.lastname: Mantry
authors.forename: Adel
authors.initials: A
authors.lastname: Bozorgzadeh
mesh_terms: D000328:Adult; D005260:Female; D016174:Hepacivirus / Q000235:genetics / Q000276:immunology; D006526:Hepatitis C / Q000473:pathology / Q000821:virology; D018937:Hepatitis C Antibodies / Q000097:blood*; D006801:Humans; D008103:Liver Cirrhosis / Q000473:pathology / Q000821:virology; D016031:Liver Transplantation / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D012367:RNA, Viral / Q000097:blood; D019562:Viral Load
chemical_list: D018937:Hepatitis C Antibodies; D012367:RNA, Viral