In 1977, the initial description of the hepatitis delta antigen (HDAg) by M. Rizzetto, was made from the examination of liver biopsies of hepatitis B virus (HBV) chronic carriers, and it was logically thought to constitute a new HBV antigen (Rizzetto et al. 1977). After its characterization as a nuclear antigen, the immunoreactive material was found to reside in particles coated with the HBV envelope proteins, and was consequently referred to as a virus-like agent that could be transmitted to chimpanzee only in the presence of HBV (Bonino et al. 1984, 1986; Rizzetto et al. 1980a). Because of this absolute requirement for HBV coinfection, it has been considered as a defective virus. The cloning of the hepatitis D virus (HDV)-associated RNA was achieved in 1986 (Chen et al. 1986; Wang et al. 1986), and the nucleotide sequence analysis revealed a genome structure that was unique among animal viruses: it was a circular, single-stranded RNA of negative polarity, with an open reading frame coding for the HDAg-associated protein, the only protein that HDV RNA is known to encode, but it lacked the coding capacity for envelope proteins. Thus, since the very early phase of its discovery, HDV has been closely associated with HBV although its genome sequence presents no homology to that of HBV.

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