A viroid is the smallest known type of infectious agent. Discovered in 1971 by pathologist Theodor Otto Diener, a viroid is a simple pathogen. It consists only of a short, single strand of circular RNA. This RNA molecule is highly structured, with extensive base-pairing that causes it to fold back on itself into a compact, rod-like shape. A viroid is a naked piece of genetic material, containing just enough information to perpetuate itself within a suitable host.
Distinguishing Viroids from Viruses
The primary distinction between a viroid and a virus lies in their composition and structure. Viruses are nucleoprotein particles, meaning they consist of genetic material, which can be either DNA or RNA, enclosed within a protective protein shell called a capsid. Viroids, however, lack this protein coat. They are composed solely of RNA.
Viroid genomes are extremely small, typically ranging from 246 to 467 nucleotides. In comparison, the smallest known viruses have genomes that are thousands of nucleotides long. A virus’s genetic material contains genes that code for the proteins it needs, including its capsid and enzymes for replication. A viroid’s RNA does not code for any proteins at all.
Mechanism of Infection and Replication
Viroids must commandeer the host cell’s molecular tools to replicate. Infection begins when a viroid enters a plant cell, often through a small wound. Once inside, the viroid makes its way to the cell’s nucleus or, in some cases, the chloroplast, depending on the specific type of viroid. There, it tricks the host’s enzymes into making copies of its RNA.
The replication process relies on a host enzyme called RNA polymerase II, which normally transcribes the cell’s DNA into messenger RNA. The viroid’s structure allows it to be recognized as a template by this polymerase, which then begins to synthesize new viroid RNA. This process occurs through rolling circle replication, where the circular viroid RNA acts as a continuous template, allowing the polymerase to move around the circle repeatedly.
This rolling action produces long, linear strands composed of multiple, head-to-tail copies of the viroid genome. These long strands are then precisely cut into individual, unit-length viroid RNAs. In some viroid families, this cleavage is performed by the viroid RNA itself, which acts as a catalytic RNA or ribozyme, while in others a host enzyme is thought to be responsible for the cutting. Finally, a host RNA ligase joins the ends of these linear molecules to form new, infectious circular viroids.
Impact on Plant Health
Currently, viroids are only known to cause diseases in plants, and they can cause significant damage to agricultural crops. The method by which these non-coding RNAs cause disease is still being researched, but a leading theory involves a plant’s natural defense system known as RNA silencing. The highly structured viroid RNA can be mistaken by the plant cell for a double-stranded RNA, triggering Dicer-like enzymes to chop it into small pieces.
These small viroid-derived RNAs can then interfere with the plant’s gene expression. By mimicking the plant’s regulatory small RNAs, they can guide the plant’s silencing machinery to target and degrade the plant’s messenger RNAs. This disruption of gene regulation leads to the visible symptoms of disease, which often include stunted growth, leaf discoloration and malformation, and reduced fruit or tuber quality.
Potato spindle tuber viroid (PSTVd), the first viroid identified, causes potatoes to become elongated and cracked. In citrus trees, Citrus exocortis viroid (CEVd) can lead to stunted growth and scaling of the bark. Other diseases like avocado sunblotch and chrysanthemum stunt also result in significant losses for growers.