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Hepatitis D
Virus classification
Group: Group V ((-)ssRNA)
Order: Unassigned
Family: Unassigned
Genus: Deltavirus
Species: Hepatitis delta virus
Hepatitis D
Classification and external resources
ICD-10 B17.0, B18.0
ICD-9 070.31
MeSH D003699

Hepatitis D, also referred to as Hepatitis D virus (HDV) and classified as Hepatitis delta virus, is a disease caused by a small circular RNA virus. HDV is considered to be a subviral satellite because it can propagate only in the presence of the Hepatitis B virus (HBV).[1] Transmission of HDV can occur either via simultaneous infection with HBV (coinfection) or via infection of an individual previously infected with HBV (superinfection).

Both superinfection and coinfection with HDV results in more severe complications compared to infection with HBV alone. These complications include a greater likelihood of experiencing liver failure in acute infections and a rapid progression to liver cirrhosis, with an increased chance of developing liver cancer in chronic infections.[2] In combination with hepatitis B virus, hepatitis D has the highest mortality rate of all the hepatitis infections of 20%.





The HDV genome exists as a negative sense, single-stranded, closed circular RNA. Because of a nucleotide sequence that is 70% self-complementary, the HDV genome forms a partially double stranded RNA structure that is described as rod-like.[3] With a genome of approximately 1700 nucleotides, HDV is the smallest "virus" known to infect animals.

It has been proposed that HDV may have originated from a class of plant viruses called viroids.[4] Evidence in support of this hypothesis stems from the fact that both HDV and viroids exist as single-stranded, closed circular RNAs that have rod-like structures. Likewise, both HDV and viroids contain RNA sequences that can assume catalytically active structures called ribozymes. During viral replication, these catalytic RNAs are required in order to produce unit length copies of the genome from longer RNA concatamers. Finally, neither HDV nor viroids encode their own polymerase. Instead, replication of HDV and viroids requires a host polymerase that can utilize RNA as a template.[5] RNA polymerase II has been implicated as the polymerase responsible for the replication of HDV.[6][7] Normally RNA polymerase II utilizes DNA as a template and produces mRNA. Consequently, if HDV indeed utilizes RNA polymerase II during replication, it would be the only known pathogen capable of using a DNA-dependent polymerase as an RNA-dependent polymerase.

Delta antigens

A significant difference between viroids and HDV is that, while viroids produce no proteins, HDV produces two proteins called the small and large delta antigens (HDAg-S and HDAg-L, respectively). These two proteins are produced from a single open reading frame. They are identical for 195 amino acids and differ only by the presence of an additional 19 amino acids at the C-terminus of HDAg-L. Despite having 90% identical sequences, these two proteins play diverging roles during the course of an infection. HDAg-S is produced in the early stages of an infection and is required for viral replication. HDAg-L, in contrast, is produced during the later stages of an infection, acts as an inhibitor of viral replication, and is required for assembly of viral particles.[8]


HDV is rare in most developed countries, and is mostly associated with intravenous drug use. However HDV is much more common in Mediterranean countries, sub-Saharan Africa, the Middle East, and countries in the northern part of South America.[9] In all, about 20 million people may be infected with HDV.[10]

See also


  1. ^ Makino S, Chang MF, Shieh CK, et al. (1987). "Molecular cloning and sequencing of a human hepatitis delta (delta) virus RNA". Nature 329 (6137): 343–6. doi:10.1038/329343a0. PMID 3627276.  
  2. ^ Fattovich G, Giustina G, Christensen E, et al. (March 2000). "Influence of hepatitis delta virus infection on morbidity and mortality in compensated cirrhosis type B. The European Concerted Action on Viral Hepatitis (Eurohep)". Gut 46 (3): 420–6. doi:10.1136/gut.46.3.420. PMID 10673308. PMC 1727859.  
  3. ^ Saldanha JA, Thomas HC, Monjardino JP (July 1990). "Cloning and sequencing of RNA of hepatitis delta virus isolated from human serum". J. Gen. Virol. 71 ( Pt 7): 1603–6. doi:10.1099/0022-1317-71-7-1603. PMID 2374010.  
  4. ^ Elena SF, Dopazo J, Flores R, Diener TO, Moya A (July 1991). "Phylogeny of viroids, viroidlike satellite RNAs, and the viroidlike domain of hepatitis delta virus RNA". Proc. Natl. Acad. Sci. U.S.A. 88 (13): 5631–4. doi:10.1073/pnas.88.13.5631. PMID 1712103. PMC 51931.  
  5. ^ Taylor JM (April 2003). "Replication of human hepatitis delta virus: recent developments". Trends Microbiol. 11 (4): 185–90. doi:10.1016/S0966-842X(03)00045-3. PMID 12706997.  
  6. ^ Lehmann E, Brueckner F, Cramer P (November 2007). "Molecular basis of RNA-dependent RNA polymerase II activity". Nature 450 (7168): 445–9. doi:10.1038/nature06290. PMID 18004386.  
  7. ^ Filipovska J, Konarska MM (January 2000). "Specific HDV RNA-templated transcription by pol II in vitro". RNA 6 (1): 41–54. doi:10.1017/S1355838200991167. PMID 10668797. PMC 1369892.  
  8. ^ Sato S, Cornillez-Ty C, Lazinski DW (August 2004). "By inhibiting replication, the large hepatitis delta antigen can indirectly regulate amber/W editing and its own expression". J. Virol. 78 (15): 8120–34. doi:10.1128/JVI.78.15.8120-8134.2004. PMID 15254184. PMC 446097.  
  9. ^ Radjef N, Gordien E, Ivaniushina V, et al. (March 2004). "Molecular phylogenetic analyses indicate a wide and ancient radiation of African hepatitis delta virus, suggesting a deltavirus genus of at least seven major clades". J. Virol. 78 (5): 2537–44. doi:10.1128/JVI.78.5.2537-2544.2004. PMID 14963156. PMC 369207.  
  10. ^ Taylor JM (January 2006). "Hepatitis delta virus". Virology 344 (1): 71–6. doi:10.1016/j.virol.2005.09.033. PMID 16364738.  

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