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Hepatitis Delta Virus RNA Editing

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Part of the Medical Intelligence Unit book series (MIUN)

Abstract

The genome of hepatitis delta virus (HDV) is the smallest known to infect man. Encoding just one protein, hepatitis delta antigen (HDAg), HDV relies heavily on host functions and on structural features of the viral RNA. A good example of this reliance is found in the process known as HDV RNA editing, which requires particular structural features in the HDV antigenome, and a host RNA editing enzyme, ADARl. During replication, the adenos-ine in the amber stop codon in the viral gene for the short form of HDAg (HDAg-S) is edited to inosine. As a result, the amber stop codon in the HDAg-S open reading frame is changed to a tryptophan codon; the reading frame is thus extended by 19 or 20 codons and the longer form of HDAg, HDAg-L, is produced. This change serves a critical purpose in the HDV replication cycle because HDAg-S supports viral RNA replication, while HDAg-L is required for virion packaging but inhibits viral RNA replication. This review will cover the mechanisms of RNA editing in the HDV replication cycle and the regulatory mechanisms by which HDV controls editing.

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Casey, J.L. (2006). Hepatitis Delta Virus RNA Editing. In: Hepatitis Delta Virus. Medical Intelligence Unit. Springer, Boston, MA. https://doi.org/10.1007/0-387-35103-5_5

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