Published online Nov 12, 2015. doi: 10.5501/wjv.v4.i4.313
Peer-review started: July 10, 2015
First decision: July 31, 2015
Revised: October 14, 2015
Accepted: October 23, 2015
Article in press: October 27, 2015
Published online: November 12, 2015
Hepatitis delta virus (HDV) is the etiologic agent of the most severe form of virus hepatitis in humans. Sharing some structural and functional properties with plant viroids, the HDV RNA contains a single open reading frame coding for the only virus protein, the Delta antigen. A number of unique features, including ribozyme activity, RNA editing, rolling-circle RNA replication, and redirection for a RNA template of host DNA-dependent RNA polymerase II, make this small pathogen an excellent model to study virus-cell interactions and RNA biology. Treatment options for chronic hepatitis Delta are scarce and ineffective. The disease burden is perhaps largely underestimated making the search for new, specific drugs, targets, and treatment strategies an important public health challenge. In this review we address the main features of virus structure, replication, and interaction with the host. Virus pathogenicity and current treatment options are discussed in the light of recent developments.
Core tip: Hepatitis delta virus (HDV) is the etiologic agent of probably the most severe form of virus hepatitis. HDV replication and spread depends on the presence of hepatitis B virus which provides the envelope proteins coded exclusively by its own genome. About 20 million people are currently chronically infected with HDV and no specific therapy is still available. Here, we review the current knowledge on HDV biology, epidemiology, pathogenesis, and treatment. Future trends and perspectives are discussed in the light of recent developments on HDV biology and its interaction with the host.