Cellular immune responses to the HBc or HBe antigen of hepatitis B vir
uses contribute to the pathogenesis of hepatitis B and to the eliminat
ion of the virus. Insufficient cytotoxic immune reactions against the
core antigen may be one major reason for viral persistence in the abse
nce of severe clinical symptoms. We attempted to stop viral. persisten
ce in the animal model of congenitally infected ducks by injection of
recombinant DHBc particles, together with the strong immunostimulator
Freund's adjuvant. However, the duck HBc antigen (DHBcAg)-treated duck
s did not develop detectable liver disease, nor was the virus persiste
nce affected. The congenitally infected ducks did not contain antibodi
es against DHBcAg before injection despite continuous production of du
ck hepatitis B virus, and developed only a weak transient antibody res
ponse after injection of recombinant DHBcAg together with Freund's adj
uvant. Noninfected ducks developed, in contrast, a strong antibody res
ponse to the injected DHBcAg. We conclude that congenitally infected d
ucks are immunotolerant to DHBcAg and cannot be cured by immunotherapy
with exogenous recombinant DHBcAg.