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. Aim: 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. Design: 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‐γ) 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. Conclusion: The sharp rise in IFN‐γ production mediated by the acute HAV infection may be pivotal in the suppression of HBV replication in chronic hepatitis B.