Viroids Are Plant Pathogens

Viroids are plant pathogens that consist of a short stretch (a few hundred nucleobases) of highly complementary, circular, single-stranded RNA without the protein coat that is typical for viruses.[1] The smallest discovered is a 220 nucleobase scRNA (small cytoplasmic RNA) associated with the rice yellow mottle sobemovirus (RYMV).[2] In comparison, the genome of the smallest known viruses capable of causing an infection by themselves are around 2kilobases in size. The human pathogen hepatitis D is similar to viroids.[3] Viroids are extremely small in size, consisting of less than 10,000 atoms.[4]
Viroids were discovered and given this name by Theodor Otto Diener, a plant pathologist at the Agricultural Research Service in Maryland, in 1971.[5][6][7]
Viroids, however, consist of only a single RNA strand. They do not code for proteins in the way that viruses do; rather, they rely for reproduction on proteins and enzymes already present in host cells. Viroids affect plants; some do not display symptoms in infected crops. Crops that may be affected by viroids include coconuts, tomatoes, potatoes, cucumbers and citrus fruits.
Viroids in Humans * Viroids do not cause disease processes in humans or animals; their effects are limited to plants. However, a similar infectious agent, a virusoid, causes type D hepatitis, an exceptionally virulent form of that disease. Virusoids are single-stranded, circular RNA molecules, like viroids, but they require a helper virus to infect. In the case of hepatitis D, the virusoid requires the protein coat of hepatitis B for
There are two variations of this rolling circle mechanism:

In the first variation (A), the circular plus strand is copied by viroid RNA-dependent RNA polymerase to form a concatameric minus strand (step 2). Site-specific cleavage (arrows) of this strand produces a monomer that is circularized by a host RNA ligase (step 3) and then copied by the RNA polymerase to produce a concatameric plus strand. Cleavage of this strand (step 5) produces monomers which, on circularization, produces the progeny circular, plus RNA, the dominant form in vivo.
In the other variation (B), the concatameric minus strand of step 1 is not cleaved but is copied directly to give a concatameric plus strand (step 3), which is cleared specifically to monomers for ligation to the circular progeny. Those RNAs that self-cleave only in the plus strand in vitro are considered to follow this