Closing Notes

HDV superinfection of chronically HBV-infected patients results in acute, sometimes severe, hepatitis and in a high frequency of persistence of both viruses. The disease could be triggered by a HDV specific CTL response, although no data on the cellular immune response in acute HDV infection has been reported so far. Cellular immune responses (Th cells and CTLs) were found in patients with resolved HDV superinfection (without detection of HDV RNA), but not in chronically HDV-infected patients. Although these results were seen only in a small number of patients, one might conclude that a proper T-cell response seems to be the prerequisite for the elimination of HDV. This mechanism was shown for chronic HBV infection: a higher frequency of HBV-specific CD8+ T-cells was detected in patients with a low level of HBV replication than in those with a high level of HBV replication (Webster et al. 2004). The HBV-specific CD8+ T-cell response was overall weak in the blood of patients with chronic HBV infections. Beside the cellular immune response a humoral one is mounted in all patients. However, antibodies are apparently not able to modulate the course of infection. Like HBcAg, HDV is encapsidated by HBsAg; therefore, antibodies to HDV are not able to neutralize the virus, comparable to the inability of anti-HBc antibodies to neutralize HBcAg.

Many questions about the immunopathogenesis of HDV still remain open. It is still unanswered whether the balance between viral load (high versus low) and the strength of the HDV-specific T-cell response play a role for the preferential establishment of either immunity or immunopathology in HDV superinfection. Cytopathic effects of HDV replication in human livers have not been finally excluded and, therefore, HDV itself may contribute to liver disease. Genetic variations during the chronic course of infection and its role for an immunevasion have also not been extensively studied so far (see the chapter by J.L. Casey and J.L. Gerin, this volume). Probably studies in the woodchuck model investigating the kinetics of the immune response and looking for immunological escape during the course of infection could give us some more insight in the immune response to HDV.

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