It is good news that even before we can understand such things as the origin of HDV, we are seeing the demise of HDV as a clinically relevant infectious agent (Gaeta et al. 2000). The number of chronic HDV carriers is decreasing, maybe largely due to decreases in the number of HBV carriers as a result of increasing vaccination programs. However, HDV remains as one of the most interesting of animal viruses. HDV has so many unique features. It also serves as an important model for studies of RNA biology. In the future we expect to see a detailed understanding of HDV RNA-directed RNA transcription. What is it about this RNA, together with help from S-HDAg, that allows such successful redirection of a host polymerase? While it may currently be very difficult to reconstitute RNA-directed transcription in vitro, a more accessible approach, already solved for other animal viruses (Qanungo et al. 2004), might be the isolation of transcription-competent replication complexes.

Acknowledgements I especially thank the following members of the lab: Jinhong Chang, Severin Gudima, and Xingcao Nie, for discussions regarding this manuscript and for allowing citation of unpublished studies. Additional constructive comments on the manuscripts were provided by Glenn Rall and Richard Katz. Also, I thank collaborators Cheng-Ming Chiang, Jack Keene, and Luiz Penalva. Funding was provided by grants AI-26522 and CA-06927 from the N.I.H., and by an appropriation from the Commonwealth of Pennsylvania.

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