Viroid

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Viroid
Virus classification
(unranked) Subviral agents
(unranked) Viroid
Families

Pospiviroidae
Avsunviroidae

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. The smallest so far is a 220 nucleobase scRNA (small cytoplasmic RNA) associated with the rice yellow mottle sobemovirus (RYMV)[1]. In comparison, the genome of the smallest known viruses capable of causing an infection by themselves are around 2 kilobases in size.

Viroid RNA does not code for any known protein; some even lack the AUG initiation codon. 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 which allow self-cleavage and ligation of unit-size genomes from larger replication intermediates. It has been proposed that viroids are "escaped introns".

Viroids are usually transmitted by seed or pollen. Infected plants can show distorted growth. 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:

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

Putative secondary structure of the PSTVd viroid
Putative secondary structure of the PSTVd viroid

Contents

[edit] Taxonomy

There is only one viroid that can infect humans, this is Hepatitis D (not mensioned above)

[edit] Viroids and RNA silencing

There has long been confusion over how viroids are able to induce symptoms on plants without encoderent 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 [2]. 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.[3]Finally, transgenic expression of the noninfectious hpRNA of potato spindle tuber viroid develop all the corresponding viroid like symptoms.[4]

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.

[edit] See also

[edit] References

  1. ^ http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9499801&dopt=Abstract
  2. ^ Elizabeth Dickson, Hugh D. Robertson, C. L. Niblett, R. K. Horst & Milton Zaitlin. Minor differences between nucleotide sequences of mild and severe strains of potato spindle tuber viroid. 1979, Nature, 277 60-62
  3. ^ Replicating potato spindle tuber viroid RNA is accompanied by short RNA fragments that are characteristic of post-transcriptional gene silencing, Nucleic Acid Research, 29, pages 2401-2408
  4. ^ Wang et al., On the role of RNA silencing in the pathogenicity and evolution of viroids and viral satellites, Proceedings of the National Academy of Science (USA), Vol. 101, pages 3275-3280

[edit] Further reading