In general, the
biological and structural properties of the hepatitis delta virus resemble those of the viroids and related
satellite RNA viruses of plants. This resemblance has been strengthened by the discovery that, in analogy to the self-cleaving of some
plant RNA viruses, hepatitis delta virus
RNA possesses autocleaving and autoligating sites located in sequences that are homologous with highly conserved domains in the viroids. The catalytic properties identify the hepatitis delta virus as the first mammalian
ribozyme. The current interpretation of the pathobiology of
delta hepatitis rests on the postulates that the hepatitis delta virus invariably requires hepatitis B virus for
infection and is highly pathogenic. Accordingly,
delta hepatitis is thought to occur when hepatitis delta virus coinfects with hepatitis B virus or when it superinfects hepatitis B virus carriers. However, new evidence from the
liver transplantation model suggests that hepatitis delta virus is capable of establishing latent,
asymptomatic infections without the apparent assistance of hepatitis B virus: in this model, disease was only reactivated when hepatitis B virus also returned to the graft. Thus, hepatitis B virus
superinfection on a latent hepatitis delta virus state may be a third pathobiological mechanism conducive to
delta hepatitis.