Keese P, Symons R H
Proc Natl Acad Sci U S A. 1985 Jul;82(14):4582-6. doi: 10.1073/pnas.82.14.4582.
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.
基于序列同源性，提出了一个关于类病毒五个结构和功能域的模型。这些结构域包括：（i）一个保守的中心区域，能够形成两种可能调控类病毒复制周期两个阶段的替代结构；（ii）一个与致病性相关的区域；（iii）一个具有高序列变异性的结构域；（iv和v）两个在不同类病毒之间可互换的末端结构域。椰子死亡类病毒的部分重复现象支持了类病毒的进化涉及结构域的RNA重排这一观点，该现象在每次感染过程中从头产生。动物病毒缺陷干扰RNA也存在类似的RNA重排，其通过某种形式的不连续转录产生。这种机制可以解释类病毒以及RNA病毒的起源，即遗传信息模块可能在RNA病原体及其宿主的RNA之间经历了反复交换。
