For some time the similarities between HDV and the plant viroids have been apparent (Taylor 1999). The two major differences are that HDV has a genome at least four times bigger than that of viroids, and this genome encodes a protein, whereas the viroids encode no known proteins. Plants can also be infected by another class of agents that are known as viroid-like satellite RNAs. These also have small single-stranded RNA genomes that are frequently circular and sometimes encode a single small protein. These virusoids might seem more similar in that they, like HDV, need a helper virus. However, for virusoids the helper function is to provide the RNA polymerase activity.

At one time it was suggested that HDV might have arisen via template-switching between a putative human viroid and a host mRNA (Brazas and Ganem 1996; Robertson 1996). This model remains unlikely for several reasons, especially since we have yet to find a single human viroid. Furthermore, it is relevant to note the following recent study (Gudima et al. 2005). A 5'-capped and 3'-polyadenylated mRNA for S-HDAg was pre-associated with a linear antigenomic RNA that lacked most of the open reading frame for S-HDAg. When these were pre-annealed and then transfected into a cell (expressing the S-HDAg) the reconstitution of replicating HDV RNA was detected. However, without this pre-annealing, there was no reconstitution. Furthermore, the linear antigenomic RNA was not able to achieve HDV reconstitution using abundant copies of DNA-directed HDV mRNA that were also present in the recipient cells.

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