Rizzetto M
Institute of Internal Medicine, University of Turin, Italy.
J Hepatol. 1990;11 Suppl 1:S145-8. doi: 10.1016/0168-8278(90)90183-r.
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.
一般来说，丁型肝炎病毒的生物学和结构特性类似于类病毒以及植物相关的卫星RNA病毒。这一相似性因以下发现而得到强化：类似于某些植物RNA病毒的自我切割，丁型肝炎病毒RNA在与类病毒高度保守结构域同源的序列中拥有自我切割和自我连接位点。这些催化特性将丁型肝炎病毒确定为首个哺乳动物核酶。目前对丁型肝炎发病机制的解释基于以下假设：丁型肝炎病毒感染始终需要乙型肝炎病毒，且具有高度致病性。因此，人们认为当丁型肝炎病毒与乙型肝炎病毒同时感染或重叠感染乙型肝炎病毒携带者时会发生丁型肝炎。然而，肝移植模型的新证据表明，丁型肝炎病毒能够在没有乙型肝炎病毒明显协助的情况下建立潜伏、无症状感染：在该模型中，只有当乙型肝炎病毒也重新回到移植物中时，疾病才会复发。因此，在潜伏性丁型肝炎病毒状态下的乙型肝炎病毒重叠感染可能是导致丁型肝炎的第三种发病机制。
