title: Outcome of liver disease and response to interferon treatment are not influenced by hepatitis B virus core gene variability in children with chronic type B hepatitis.
abstract: OBJECTIVE
  Hepatitis B virus (HBV) core gene heterogeneity may influence the outcome of liver disease and the response to interferon (IFN) therapy in adult HBV carriers. The aim of this study was to evaluate the possible association between HBV core gene variability and evolution of chronic hepatitis in children.
  
  
  METHODS
  We examined serum samples from 25 children with HBV chronic hepatitis and HBe antigen (HBeAg) positivity who were followed-up for a mean of 7.4 years. Seven cases spontaneously seroconverted to anti-HBe, becoming HBV healthy carriers; nine cases were successfully treated with IFN; nine cases were non-responders to IFN therapy. HBV-DNA was extracted from one serum sample ("I") collected during the HBeAg positive phase, and from a second sample ("II") collected after the anti-HBe seroconversion or, in non-responders, after stopping therapy. The entire core gene of the HBV isolates was amplified and sequenced.
  
  
  RESULTS
  Each isolate showed single or no missense mutation independently of the clinical behavior of the patients. HBeAg-defective viruses were detected in one case in both samples and in two cases only in sample "II".
  
  
  CONCLUSIONS
  Core gene variability does not seem to be involved either in the outcome of infection or in the response to IFN treatment in children with HBV chronic hepatitis. Considering that most of the HBV carriers in our area acquire the infection in childhood, our data suggest that core gene heterogeneity is not a major cause of progression to chronicity.
authors.affiliation: Dipartimento di Medicina Interna, Universita di Messina, Italy.
authors.forename: F
authors.initials: F
authors.lastname: Schepis
authors.forename: G
authors.initials: G
authors.lastname: Verucchi
authors.forename: T
authors.initials: T
authors.lastname: Pollicino
authors.forename: L
authors.initials: L
authors.lastname: Attard
authors.forename: S
authors.initials: S
authors.lastname: Brancatelli
authors.forename: G
authors.initials: G
authors.lastname: Longo
authors.forename: G
authors.initials: G
authors.lastname: Raimondo
mesh_terms: D000293:Adolescent; D000998:Antiviral Agents / Q000627:therapeutic use*; D002353:Carrier State; D002648:Child; D002675:Child, Preschool; D002908:Chronic Disease; D004279:DNA, Viral / Q000032:analysis; D005260:Female; D014644:Genetic Variation; D016679:Genome, Viral; D006509:Hepatitis B / Q000628:therapy*; D006513:Hepatitis B e Antigens / Q000032:analysis; D006515:Hepatitis B virus / Q000235:genetics*; D006801:Humans; D007223:Infant; D007372:Interferons / Q000627:therapeutic use*; D008297:Male; D009154:Mutation; D016896:Treatment Outcome; D014758:Viral Core Proteins / Q000235:genetics
chemical_list: D000998:Antiviral Agents; D004279:DNA, Viral; D006513:Hepatitis B e Antigens; D014758:Viral Core Proteins; D007372:Interferons