title: High viral load and mild liver injury in children with hemophilia compared with other children with chronic hepatitis C virus infection.
abstract: BACKGROUND
  In adults with hepatitis C virus (HCV) infection, the severity of liver disease may be influenced by the mode of transmission. The purpose of this study was to evaluate whether the mode of transmission affects liver injury and viral load in children with chronic HCV infection, independent of duration of infection and/or HCV genotype.
  
  
  METHODS
  Thirty-nine anti-HCV (EIA-2) positive patients, were divided into three groups: group 1, children with a history of blood transfusion (n = 9; age, 13.3+/-1.3 years), group 2, children with hemophilia (n = 19; age, 11.6+/-0.8 years); and group 3, children with maternal-fetal transmitted disease (n = 10; age, 4.7+/-1.1 years). Serum alanine aminotransferase, HCV viral load, HCV genotype, and liver histology were assessed.
  
  
  RESULTS
  Serum HCV viral load was higher in group 2 (4.27+/-1.0x10(6) copies/ml; p = 0.006) than in group 1 (0.73+/-0.3x10(6) copies/ml) and in group 3 (0.83+/-0.2x10(6) copies/ml). Conversely, group 2 had less severe liver injury compared with children of similar age in group 1 (p = 0.022). Despite a shorter duration of infection, group 3 had liver injury similar to that in group 1. Hepatitis C virus genotype did not influence the level of viremia or liver injury.
  
  
  CONCLUSIONS
  Although children with hemophilia exhibited a high HCV viral load, liver histopathology was less severe than in children who had acquired HCV by blood transfusion or maternal-fetal transmission. These observations support the need to investigate the role of host immune response rather than the virus per se in the pathogenesis of HCV infection in children.
authors.affiliation: Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
authors.forename: A
authors.initials: A
authors.lastname: Zellos
authors.forename: D L
authors.initials: DL
authors.lastname: Thomas
authors.forename: C
authors.initials: C
authors.lastname: Mocilnikar
authors.forename: E J
authors.initials: EJ
authors.lastname: Perlman
authors.forename: J K
authors.initials: JK
authors.lastname: Boitnott
authors.forename: J F
authors.initials: JF
authors.lastname: Casella
authors.forename: K B
authors.initials: KB
authors.lastname: Schwarz
mesh_terms: D000293:Adolescent; D002648:Child; D002675:Child, Preschool; D005260:Female; D006467:Hemophilia A / Q000473:pathology / Q000821:virology*; D006526:Hepatitis C / Q000635:transmission; D019698:Hepatitis C, Chronic / Q000473:pathology / Q000821:virology*; D006801:Humans; D008099:Liver / Q000473:pathology*; D008297:Male; D008431:Maternal-Fetal Exchange; D011247:Pregnancy; D065227:Transfusion Reaction; D019562:Viral Load