Hepatitis D, and hepatitis D virus (HDV), and are classified into delta hepatitis virus, is a disease caused by RNA viruses of the sheath small circular. Since it can be dispersed in the presence of hepatitis B virus only (HBV), and ideas E HDV subviral satellite B, C, and D: It is one of the hepatitis virus five known. Transmission of HDV, it may be caused by one of the co-infection and background (superinfection) carrier status of hepatitis B or chronic hepatitis B or HBV (superinfection). Compared to the infection of HBV alone, co-infection and co-infected with HDV results in complications more serious. The complications of these, likely to develop liver failure, the rapid progression and acute infection cirrhosis of the liver, an increased risk of liver cancer in chronic infection is high. In combination with hepatitis B virus, D-Shaped hepatitis has a high mortality rate of all HCV infection of 20%.

Receptors that recognize HDV human hepatocytes has not been established, it is believed to have an outer layer of single, two viruses, is the same as the HBV receptor. HDV to recognize the receptor N-terminal domain by a large HBs antigen, hepatitis B surface antigen. Mapping by mutagenesis in this region, the amino acid residues constitute 9-15 receptor binding site is shown. Move nucleocapsid to the nucleus by the signal from the nucleocapsid that does not contain the RNA polymerase to replicate the viral genome, HDAg makes use of the RNA polymerase of the cell the virus after the introduction of liver cells, the virus is uncoated. First, the addition III RNA Pol II, and RNA polymerase I, generally shown to be involved in the replication of the HDV RNA using polymerase II as a template DNA and mRNA are produced now.

Therefore, when using the HDV RNA polymerase II during playback Indeed, the RNA-dependent polymerases such, become pathogens only animal known to use a DNA-dependent polymerase. Structure of the rod-like as is the cause, RNA polymerase dealing with RNA genome is collapsed, the RNA genome of circular double-stranded DNA-inch, polyadenylation and the anti-genomic RNA round additional three forms of RNA is performed linear anti-genomic RNA framework of HDAg because it is the mRNA containing an open reading. Synthesis of genomic RNA while went to nucleoplasm mediated RNA polymerase II, the synthesis of anti-genomic RNA occurs in the nucleolus mediated RNA polymerase I. HDV genomic RNA is first synthesized as a linear RNA containing multiple copies. Antigenome RNA genome and comprises a sequence of 85 nucleotides that act as a ribozyme that cleaves the RNA monomers linear independent. Then, these monomers are coupled to form a circular RNA. There are eight reported genotypes of HDV to changes of unknown cause in the pathogenicity and geographical distribution.

Significant difference does not produce virus-like protein between the HDV and viroids, it is that HDV, protein, i.e. that HDAg that are known. Two forms, it is the small HDAg of 24kDa and 27kDa large HDAg. N-terminus of the two forms is the same that additional amino acids 19 is different to the C-terminus of the large HDAg. In general, both isoforms were produced in the same reading frame containing a UAG stop codon at codon 196 that generates HDAg slight. However, the termination codon of change UCG -1 large HDAg editing adenosine deaminase of cellular enzymes to allow production,. Has 90% sequence identity, two proteins of these different roles during infection. By entering the nucleus and is produced in the early stages of infection, HDAg-S supports the viral replication. HDAg-L, on the contrary, is produced during the later stages of infection, it acts as an inhibitor of viral replication, assembly of virus particles is required. The RNA is edited by cellular enzymes like this is to adjust the balance between virion assembly and replication of the virus, it is important for the viral life cycle.