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Editing efficiency of hepatitis delta virus RNA is related to the course of infection in woodchucks

Ailing Yang

Department of Medicine, Q.E.Q.M. Wing, St Mary's Hospital Medical School, Imperial College of Science, Technology and Medicine, London W2 1NY, UK

Based on evidence in vitro which shows that the small form of hepatitis delta virus (HDV) antigen (S-HDAg) initiates virus replication, whereas the long form (L-HDAg) encoded by the edited L-genome inhibits replication, we first put forward the hypothesis that HDV RNA editing efficiency, i.e. the intracellular L/S-genome ratio, could be a determining factor on the course of the infection. In order to analyse the precise sequence of events after infection, woodchuck carriers of woodchuck hepatitis virus (WHV) were superinfected with HDV and sequential changes in HDV RNA editing efficiency were analysed in relation to the duration of viraemia. Our findings show that: (1) in both transiently and persistently viraemic woodchucks, the percentage of L-genome is higher at the early stage of onset of the disease than at the late stage; (2) at the early stage of onset the percentage of L-genome is higher in cases with transient viraemia than in those with persistent viraemia; (3) a relatively greater decrease in L-genome is seen later in transiently viraemic animals than in those that remain persistently viraemic. In view of the above findings in vivo and other supporting evidence in vitro, we propose a hypothesis for the pathogenesis of HDV. This hypothesis predicts the outcome of acute infection and we suggest a gene therapeutic approach to this disease based on the intracellular accumulation (or increase) of the L-genome.

^* Author for correspondence. Fax +44 171 724 9369.

Present address: Division of Virology, National Institute for Biological Standards and Control, Blanche Lane, South Mimms, Herts EN6 3QG, UK.

Received 16 March 1995; accepted 18 August 1995.

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