On the basis of sequence homology a model is proposed for five structural and 
functional domains in viroids. These domains include (i) a conserved central 
region capable of forming two alternative structures that may regulate two 
phases of the viroid replication cycle, (ii) a region associated with 
pathogenicity, (iii) a domain with high sequence variability, (iv and v) two 
terminal domains that are interchangeable between viroids. That the evolution of 
viroids has involved RNA rearrangements of domains is supported by the partial 
duplication of coconut cadang cadang viroid, which arises de novo during each 
infection. Similar RNA rearrangements have been established for animal viral 
defective interfering RNAs, which arise by some form of discontinuous 
transcription. This mechanism could account for the origin of viroids and also 
RNA viruses, whereby modules of genetic information may have undergone repeated 
exchange between RNA pathogens and the RNA of their hosts.