title: Suppression of hepatitis B virus replication mediated by hepatitis A-induced cytokine production.
abstract: BACKGROUND
  Acute hepatitis A virus (HAV) infection can cause severe hepatitis especially in patients with underlying chronic liver disease. In patients with pre-existing chronic hepatitis B (HBV) acute HAV infection can suppress HBV replication. The exact mechanism of HBV suppression during acute HAV infection is still a subject of debate. One mechanism may be the production of HAV infection-induced cytokines leading to suppression of HBV replication and viral clearance.
  
  
  OBJECTIVE
  To evaluate cytokine production and HBV-specific lympho-proliferative responses (LPR) during acute HAV infection in a patient with chronic HBV infection-clearing markers of active HBV replication.
  
  
  METHODS
  Early detection of a case of acute HAV infection in an HBeAg-positive, HBV DNA-positive chronic HBV patient treated with lamivudine.
  
  
  RESULTS
  At the time of HAV infection a sharp peak in the gamma-interferon (IFN-gamma) level occurred just before the rise in serum transaminase activity. This was subsequently followed by a decrease in HBV DNA and HBeAg below the limit of detection of the assay. However the HBV-specific T-cell response was not modified. After resolution of the acute HAV infection and withdrawal of antiviral therapy HBV replication relapsed.
  
  
  CONCLUSIONS
  The sharp rise in IFN-gamma production mediated by the acute HAV infection may be pivotal in the suppression of HBV replication in chronic hepatitis B.
authors.affiliation: Department of Hepatogastroenterology, Erasmus University Hospital Rotterdam, The Netherlands.
authors.forename: A B
authors.initials: AB
authors.lastname: van Nunen
authors.forename: O
authors.initials: O
authors.lastname: Pontesilli
authors.forename: F
authors.initials: F
authors.lastname: Uytdehaag
authors.forename: A D
authors.initials: AD
authors.lastname: Osterhaus
authors.forename: R A
authors.initials: RA
authors.lastname: de Man
mesh_terms: D000208:Acute Disease; D000998:Antiviral Agents / Q000627:therapeutic use; D002478:Cells, Cultured; D004279:DNA, Viral / Q000032:analysis; D006506:Hepatitis A / Q000097:blood / Q000276:immunology*; D006512:Hepatitis B Core Antigens / Q000097:blood; D006515:Hepatitis B virus / Q000235:genetics / Q000254:growth & development* / Q000276:immunology / Q000302:isolation & purification; D019694:Hepatitis B, Chronic / Q000188:drug therapy / Q000276:immunology*; D006507:Hepatovirus / Q000276:immunology* / Q000302:isolation & purification; D006801:Humans; D007371:Interferon-gamma / Q000096:biosynthesis*; D019259:Lamivudine / Q000627:therapeutic use; D008213:Lymphocyte Activation / Q000276:immunology; D008297:Male; D015163:Superinfection / Q000276:immunology; D014762:Viral Interference / Q000276:immunology*; D014779:Virus Replication
chemical_list: D000998:Antiviral Agents; D004279:DNA, Viral; D006512:Hepatitis B Core Antigens; D019259:Lamivudine; D007371:Interferon-gamma