Viroid pathogenesis

The small size and noncoding nature of viroid RNAs raises intriguing and specific questions about how they induce disease. The absence of viroid-encoded proteins, in sharp contrast to viruses, led originally to the assumption that viroid diseases were the result of direct interaction of the genomic viroid RNA (or its complement) with cellular constituents. Recently, however, the possible involvement of indirect interactions via RNA silencing and other existing regulatory networks has received increasing attention. This chapter summarizes early views and discusses newly available evidence that RNA silencing directed by viroid-derived small RNAs inhibits, at least in some cases, both the spread of viroid infection and the expression of key host genes that ultimately may result in symptom induction. Viroid infection is also accompanied by changes in the levels of certain microRNAs as well as other host-encoded small RNAs derived from ribosomal RNA transcripts. Clearly, viroid pathogenesis engages multiple regulatory networks, thus demanding network-based experimental strategies to complement the current gene-by-gene approaches.