The prevention of HDV infection can readily be achieved by immunisation with the envelope proteins (HBsAg/pre-S) of the helper virus (HBV) on which HDV is dependent. In patients with established chronic HBV infection, superinfection with HDV may theoretically be controlled, but not prevented, by immunisation to the internal components of HDV which may be the target of a cytotoxic T-cell response to HDV infected hepatocytes. Such a response, by analogy to the effects of immunisation to HBcAg, may result in rapid lysis of infected hepatocytes thereby limiting the spread of HDV through the liver. In our preliminary experiments using recombinant HDAg (amino-acids 13-76) we have shown that a humoral immune response to HDV prior to HDV superinfection, does not control HDV infection but may facilitate it. We do not know whether this immunisation protocol successfully induced a cytotoxic T-cell response or whether the region of HDAg included is recognised by cytotoxic T-cells and involved in the immune destruction of HDV infected cells. Further studies of the mechanisms of lysis of HDV infected hepatocytes to determine the role, if any, of cytotoxic T-cells or humoral lytic mechanisms, is needed. Although short courses of alpha interferon inhibit HDV replication, relapses are common and amelioration of the inflammatory liver disease is not always seen. Longer periods of therapy may be effective if they can be continued until clearance of the helper virus (HBV), as well as HDV, has occurred. In three patients treated for greater than one year, clearance of HBsAg has occurred. If these patients remain in this state after stopping therapy, further studies of long term alpha interferon therapy may be fruitful.
|Number of pages||7|
|Journal||Progress in clinical and biological research|
|Publication status||Published - 1991|