Theodor Diener's 1971 discovery of viroids was hard sell. The now-retired Diener, who was working as a plant pathologist with the Agricultural Research Service in Maryland, was trying to isolate the infectious agent responsible for potato spindle tuber disease. He presumed it was a virus. Instead, he detected a novel pathogen, which, unlike viruses, was not protected by a protein coat and appeared to comprise a single RNA molecule.1
Many investigators weren't convinced that the hypothesized entity was big enough to replicate, let alone cause disease. Not until electron microscopy allowed scientists to actually see one of these tiny pathogens, which are about one-fiftieth the size of the smallest virus, did the scientific community seriously consider the viroid.
© Federation of the European Biochemical Societies
At top is the rod like secondary structure proposed for the
Now, viroids are among the best-studied RNA molecules.2 Approximately 30 known viroid species and hundreds of variants exist. They cause disease in more than two dozen crop plants, from chrysanthemums to coconuts. Viroids are classified into two major families: the
Although viroid diseases often resemble viral infections, the similarities stop there. Not only are the single-stranded, singular RNAs, which range in size from 250 to 400 nucleotides, unprotected by any protein coat, but they also have no functional open-reading frame. So, unlike viral RNAs, viroids do not encode any proteins. This raises several questions: How do viroids cause disease? How do they replicate without the aid of a helper virus? And how do they move from cell to cell and host to host? Their self-complementary, circular nature and secondary structure (which allow viroids to self-cleave) provide some answers. Most recently, the identification of viroid-specific small interfering RNAs has led investigators to believe that RNA silencing also plays a role (see story
- Leslie A. Pray