Updated: February 11, 2007

Hepatitis D (δ):

In 1977, a novel nuclear antigen was discovered in patients with chronic HBV infection - called delta antigen (δ) (after the 3 known HBV antigens). By 1980, transmission experiments in chimpanzees showed that HDV was a defective transmissible pathogen dependent on HBV for replication - similar to plant virus satellite RNAs. Delta antigen is found wherever HBV infection occurs and seems to potentiate the pathogenic effects of HBV infection. Fulminant hepatitis (mortality ~80%) is 10 times more common than with HBV infection alone. Patients with dual infection with hepatitis B virus (HBV) and delta virus (HDV) respond poorly to interferon (IFN) therapy. Liver transplantation for HDV cirrhosis seems to be more successful than in any other viral hepatitis, with comparatively few reinfections of the grafted liver.
The HDV genome is a unique chimaeric molecule with some of the properties of a satellite virus and some of a viroid - a covalently closed circular RNA molecule 1679-1683 bases long with a branched or rod-like configuration, and taxonomically, has now been placed in its own group within the class V negative sense RNA viruses, Deltavirus:

This molecule is thought to be replicated by host cell RNA polymerase II using a rolling circle mechanism. This produces linear concatemers which must be cleaved for infectivity. The cleavage is carried out by a ribozyme domain present in the HDV RNA, the only known example of a ribozyme in an animal virus genome ("Crystal structure of a hepatitis delta virus ribozyme" Nature 395: 567-574, 1998).

However, unlike all other viroids, HDV encodes a protein, the delta antigen, which is a nuclear phosphoprotein. Post-transcriptional RNA editing results in the production of two slightly different forms of the protein, S-HDAg (195 amino acids) which is necessary for HDV replication and L-HDAg (214 amino acids) which is necessary for the assembly and release of HDV-containing particles. Preparations from HDV-infected animals contain heterologous particles distinct from HBV but with ill-defined structure. L-HDAg and small-form hepatitis B surface antigen (HBsAg) of the helper hepatitis B virus have previously been shown to be the minimum components for the assembly of these particles. Replication of human hepatitis delta virus: recent developments. Trends Microbiol. 2003 11: 185-190.

HDV Infection

Replication of HDV is hard to study since it requires the presence of a helper virus (HBV) which itself cannot be cultured! HDV can be controlled by controlling HBV infection. The worldwide distributions of HDV infection is currently changing as HBV vaccination programmes begin to take effect: Gaeta GB. et al. (2000) Chronic hepatitis D: a vanishing disease? An Italian multicenter study. Hepatology 32: 824–827.

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