What are Viroids?

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Viroids are plant pathogens consist of a small single-stranded RNA particles that infect plants and cause diseases. Viroids are smaller than virus and are not enclosed in any protein coat. In 1971, viroids were discovered by “Theodor Otto Diener”, a plant pathologist at the Agricultural Research Service in Maryland. Viroids are 80 times smaller than typical viruses. The human pathogen hepatitis D is similar to viroids. Viroids are catalytic RNA’s(ribozomes) split RNA to produce fragments containing a 5’ hydroxyl and 2’, 3’-cyclic phosphate. This is a nonhydruatlytic reaction which plays an important role in the replication of these RNAs in vivo. These are all intramolecular reactions with single turnover. Viroid RNA does not code for any protein.

What is the structure of viroid?

The members of the family Pospiviroidae, whose type species is Potato spindle tuber viroid (PSTVd). The first described viroid has a characteristic central conserved region (CCR) and a terminal conserved region(TCR), or a terminal conserved hairpin(TCH). The sequence of the CCR and the presence or absence of TCR and TCH allocate members of this family to five genera. The other four viroids do not have these conserved themes and are classified within the family of Avsunviroidae, whose species type is Avocado sunblotch viroid (ASBVd), on the basis of their ability to form hammerhead structures. There is sound evidence that PSTVd adopt in vitro a typical rod-like secondary structure formed by alternating short double-stranded regions and single-stranded loops. The repititions and deletions observed in certain viroids always preserve the rod-like structure.

The rod-like structure has been divided into five structural/functional domains. They are central (C), pathogenic (P), variable (V), terminal right (TR) and terminal left (TL). The central conserved region (CCR) is located within the C domain and the TCR and TCH within the TL domain. The structural domains are related to specific functions: The C domain, mainly the upper strand of the CCR is involved in the cleavage and ligation of the multimeric PSTVd RNA. Some conserved regions like, the TCR and TCH, still wait for a function.

How do viroids replicate?

It involves a RNA based rolling-circle mechanism. Viroids are associated with the cell nuclei mainly the chromatin, and possibly with the endomembrane system of the host cell. Viroids replicate by direct RNA copying .The components required for viroid replication including the RNA polymerase are provided by the host. Viroids are small non-coding, circular RNAs able to replicate autonomously in certain plants. The host RNA polymerases  are supported by additional host proteins, start transcription from definite sites indicating the existence of viroid promoters.

The replication mechanism involves RNA-based rolling-circle mechanism with three steps:

• Synthesis of longer-than- unit strands catalyzed by either the nuclear RNA polymerase II or a nuclear-encoded chroloplastic RNA polymerase redirected to transcribe RNA templates.

• Cleavage to unit-length, which in the family Avsunviroidae to intervene by hammered ribozomes enclosed in polarity strands, while in the family Pospiviroidae probably catalyzed by an RNase III-like enzyme and an RNA ligase able to circularize 5’ and 3’ termini.

•  Circularization

The only human disease caused by a viroid is hepatitis D. This disease is caused by a virus called delta agent. Delta agent is a viroid enclosed in a hepatitis B virus capsid. Hepatitis D occurs due to simultaneous infection of a cell with both the hepatitis B and hepatitis D viroid. There is a necessary interrelationship between the hepatitis D viroid RNA and human liver cell 7S RNA, the small cytoplasmic RNA which is the component of signal recognition particle, the structure involved in the secretory and membrane-associated particles. The hepatitis D viroid causes liver cell death by setting apart this 7S RNA or cleaving it.