title: Plasma interferon-gamma-inducible protein-10 levels are associated with early, but not sustained virological response during treatment of acute or early chronic HCV infection.
abstract: BACKGROUND
  High plasma levels of interferon-gamma inducible protein-10 (IP-10) have been shown to be associated with impaired treatment response in chronic hepatitis C virus (HCV) infection. Whether IP-10 levels predict treatment in acute HCV infection is unknown.
  
  
  METHODS
  Patients with acute or early chronic HCV infection from the Australian Trial in Acute Hepatitis C (ATAHC) cohort were evaluated. Baseline and on-treatment plasma IP-10 levels were measured by ELISA. IL28B genotype was determined by sequencing.
  
  
  RESULTS
  Overall, 74 HCV mono-infected and 35 HIV/HCV co-infected patients were treated in ATAHC, of whom 89 were adherent to therapy and were included for analysis. IP-10 levels correlated with HCV RNA levels at baseline (r = 0.48, P<0.001) and during treatment. Baseline IP-10 levels were higher in patients who failed to achieve rapid virological response (RVR). Only one patient with a plasma IP-10 level >600 pg/mL achieved RVR. There was no association with IP-10 levels and early virological response (EVR) or sustained virological response (SVR).
  
  
  CONCLUSIONS
  Baseline IP-10 levels are associated with early viral kinetics but not ultimate treatment outcome in acute HCV infection. Given previous data showing that patients with high baseline IP-10 are unlikely to spontaneously clear acute HCV infection, they should be prioritized for early antiviral therapy.
authors.affiliation: Toronto Centre for Liver Disease, McLaughlin-Rotman Centre for Global Health, University of Toronto, Toronto, Canada.
authors.forename: Jordan J
authors.initials: JJ
authors.lastname: Feld
authors.forename: Jason
authors.initials: J
authors.lastname: Grebely
authors.forename: Gail V
authors.initials: GV
authors.lastname: Matthews
authors.forename: Tanya
authors.initials: T
authors.lastname: Applegate
authors.forename: Margaret
authors.initials: M
authors.lastname: Hellard
authors.forename: Alana
authors.initials: A
authors.lastname: Sherker
authors.forename: Vera
authors.initials: V
authors.lastname: Cherepanov
authors.forename: Kathy
authors.initials: K
authors.lastname: Petoumenos
authors.forename: Barbara
authors.initials: B
authors.lastname: Yeung
authors.forename: John M
authors.initials: JM
authors.lastname: Kaldor
authors.forename: Andrew R
authors.initials: AR
authors.lastname: Lloyd
authors.forename: Gregory J
authors.initials: GJ
authors.lastname: Dore
mesh_terms: D000208:Acute Disease; D000328:Adult; D000998:Antiviral Agents / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D054357:Chemokine CXCL10 / Q000097:blood*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D015658:HIV Infections / Q000150:complications; D019698:Hepatitis C, Chronic / Q000097:blood / Q000150:complications / Q000188:drug therapy* / Q000821:virology; D006801:Humans; D016898:Interferon-alpha / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D011092:Polyethylene Glycols / Q000627:therapeutic use*; D012367:RNA, Viral / Q000097:blood; D011994:Recombinant Proteins / Q000627:therapeutic use; D012254:Ribavirin / Q000627:therapeutic use*; D016896:Treatment Outcome; D019562:Viral Load
chemical_list: D000998:Antiviral Agents; D015415:Biomarkers; C114753:CXCL10 protein, human; D054357:Chemokine CXCL10; D016898:Interferon-alpha; D012367:RNA, Viral; D011994:Recombinant Proteins; D011092:Polyethylene Glycols; D012254:Ribavirin; C100416:peginterferon alfa-2a