HDV Disease Burden

It has been estimated that at least 15 million of the over 300 million people infected with hepatitis B virus (HBV) also harbor a hepatitis delta virus (HDV) infection and such infections can be found throughout the world (Gerin et al. 2001; Rizzetto et al. 1991). The clinical course associated with HDV is typically more severe than for HBV infection alone. Unfortunately, current therapies are largely ineffective against HDV. The study of HDV molecular virology, however, has revealed exciting new avenues for potential therapeutic intervention. After a brief review of the basic HDV virion composition and life cycle(coveredinmoredetailinother chapters in this volume),thischapter will focus on a special post-translational modification of a key HDV protein. This modification reaction, termed prenylation, turns out to be both a mechanism exploited by the virus to mediate its assembly, and the basis for an exciting new form of antiviral therapy.

HDV can be viewed as a 'parasite virus' of HBV. HDV has its own genome and encodes its own core-like protein, but it requires HBV to provide a source of envelope protein. This provides a molecular explanation for why natural HDV infections are always found in association with hepatitis B. There are two major clinical scenarios: (1) coinfection-acute simultaneous infection of HDV with HBV in a previously uninfected patient; and (2) superinfection-HDV infection of a chronically infected HBV patient (Hoofnagle 1989). This is often manifested by a sudden worsening or 'flare' of previously stable chronic HBV disease.

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