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Everything about Viroid totally explained

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's typical for viruses. The smallest so far is a 220 nucleobase scRNA (small cytoplasmic RNA) associated with the rice yellow mottle sobemovirus (RYMV). In comparison, the genome of the smallest known viruses capable of causing an infection by themselves are around 2 kilobases in size. The human pathogen hepatitis D is similar to viroids.
   Viroids were discovered and given this name by Theodor O. Diener, a plant pathologist at the Agricultural Research Service in Maryland, in 1971.
   Viroid RNA doesn't code for any protein. The replication mechanism involves interaction with RNA polymerase II, an enzyme normally associated with synthesis of messenger RNA but now using the viroid's RNA as template instead of DNA, and "rolling circle" synthesis of new RNA. Some viroids are ribozymes, having catalytic properties which allow self-cleavage and ligation of unit-size genomes from larger replication intermediates.
   The first viroid to be identified was the potato spindle tuber viroid (PSTVd). Some 33 species have been identified.
   Primary and secondary structure of the PSTVd viroid:
Primary Structure

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
Secondary Structure

Taxonomy

Viroids and RNA silencing

There has long been confusion over how viroids are able to induce symptoms in plants without encoding any protein products within their sequences. Evidence now suggests that RNA silencing is involved in the process. First, changes to the viroid genome can dramatically alter its virulence. This reflects the 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. Finally, transgenic expression of the noninfectious hpRNA of potato spindle tuber viroid develops all the corresponding viroid like symptoms.
   This evidence indicates that when viroids replicate via a double stranded intermediate RNA, they're 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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