Surveys in the 1980s showed that the hepatitis D virus (HDV) is endemic worldwide, though with prevalences and patterns of infection varying in different areas. Medical scrutiny confirmed that chronic hepatitis D usually runs a severe and progressive course, the prototype patient having HBsAg in blood, elevated ALT, a liver biopsy exhibiting aggressive hepatitis and markers of HDV (but no marker of HBV replication in serum). Although the circulation of HDV has declined significantly following the control of HBV achieved over the last 20 years, depriving HDV of the HBV network necessary to propagate its infection, there is still a consistent reservoir of the virus in Europe, sustained by two different pools of HDV-infected patients: the residual ageing domestic pool that survived the brunt of the hepatitis D epidemic in the 1970s and 1980s and the population of young patients with recent HDV infections migrating to Europe. Therapy of hepatitis D remains an unsolved business. The therapy available today is not different from the limited interferon treatment attempted more than 20 years ago. The problem is formidable as HDV has no enzymatic protein to be targeted by conventional antiviral therapy. A potential target of therapy is offered by the process of hepatitis D virion assembly.
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