A viroid is a submicroscopic infectious agent, smaller than a virus, that consists of a short section (a few hundred nucleobases) of highly complementary, circular, single-stranded RNA without the protective protein coat that is typical for viruses. They are known to cause important diseases in plants. The nucleic acid is not known to code for specific proteins, but viroids can replicate themselves by using host enzymes.
Viroids were discovered and given this name by Theodor O. Diener, a plant pathologist at the Agricultural Research Service in Maryland, in 1971 (ARS 1989; OU 2007). Until this discovery, the scientific dogma was that an entity without a protective protein coat could not replicate itself, even with the support of the host cell, and that one as small as the potato spindle tuber viroid was not supposed to be able to infect anything (OU 2007).
Viroids consist of short strands of the nucleic acid RNA without a protein coat. They lack any DNA. Viroids differ from viruses in that viruses, at their most basic level, consist of genetic material (DNA or RNA) contained within a protective protein shell. Viroids differ from prions, another type of subviral infectious agent, in that prions are made only of protein, lacking nucleic acid.
The smallest viroid identified so far is a 220 nucleobase scRNA (small cytoplasmic RNA) associated with the rice yellow mottle sobemovirus (RYMV) (Collins et al. 1998). In comparison, the genome of the smallest known viruses capable of causing an infection by themselves are around two kilobases in size. Many viroids consist of only 300 to 400 nucleotides.
Viroid RNA does not code for any known protein; some even lack the AUG initiation codon. Nonetheless, they replicate autonomously in host cells. The replication mechanism involves interaction with RNA polymerase II, an enzyme normally associated with synthesis of messenger RNA, and "rolling circle" synthesis of new RNA. Some viroids are ribozymes, having RNA enzyme properties that allow self-cleavage and ligation of unit-size genomes from larger replication intermediates. It has been proposed that viroids are "escaped introns."
Not all viroids are known to be pathogenic, but some are serious pathogens of plants. Viroids are usually transmitted by seed or pollen, but may be transported by farm implements as well. Infected plants can show distorted growth and sometimes are killed by the viroid.
Although viroids by themselves have been identified as an animal pathogen, there is support for the view that hepatitis D is traced to a viroid (Biotecnika 2005). Previously, hepatitis D was tied to a virus called delta agent, but delta agent appears to be a viroid enclosed in a hepatitis B virus capsid (Biotecnika 2005). Hepatitis D thus requires simultaneous infection of a cell with both the viroid and the hepatitis B virus.
The first viroid to be identified was the Potato spindle tuber viroid (PSTVd). Some 33 species of viroids have been identified.
PSTVd is commonly used in research experiments in viroids. A total of 359 nucleotides are included in this viroid (Davis et al. 1999).
Primary and secondary structure of the PSTVd viroid:
1 CGGAACUAAA CUCGUGGUUC CUGUGGUUCA CACCUGACCU CCUGAGCAGA AAAGAAAAAA
61 GAAGGCGGCU CGGAGGAGCG CUUCAGGGAU CCCCGGGGAA ACCUGGAGCG AACUGGCAAA
121 AAAGGACGGU GGGGAGUGCC CAGCGGCCGA CAGGAGUAAU UCCCGCCGAA ACAGGGUUUU
181 CACCCUUCCU UUCUUCGGGU GUCCUUCCUC GCGCCCGCAG GACCACCCCU CGCCCCCUUU
241 GCGCUGUCGC UUCGGCUACU ACCCGGUGGA AACAACUGAA GCUCCCGAGA ACCGCUUUUU
301 CUCUAUCUUA CUUGCUUCGG GGCGAGGGUG UUUAGCCCUU GGAACCGCAG UUGGUUCCU
There has long been confusion over how viroids are able to induce symptoms on plants without encoding any protein products within their sequences. Evidence now suggests that RNA silencing is involved in the process.
Firstly, changes to the viroid genome can dramatically alter its virulence (Dickson et al. 1979). This reflects that fact that any siRNAs produced would have less complementary base pairing with target messenger RNA. Secondly, siRNAs corresponding to sequences from viroid genomes have been isolated from infected plants (Papaefthimiou et al. 2001). Finally, transgenic expression of the noninfectious hpRNA of potato spindle tuber viroid develop all the corresponding viroid like symptoms (Wang et al. 2004).
This evidence indicates that when viroids replicate via a double stranded intermediate RNA, they are targeted by a dicer enzyme and cleaved into siRNAs that are then loaded onto the RNA-induced silencing complex. The viroid siRNAs actually contain sequences capable of complementary base pairing with the plant's own messenger RNAs and induction of degradation or inhibition of translation is what causes the classic viroid symptoms.
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