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Four additional viroids or viroid-like RNA particles were discovered between 2009 and 2015.<ref name="pmid26047558">{{cite journal |vauthors=Wu Q, Ding SW, Zhang Y, Zhu S |title=Identification of viruses and viroids by next-generation sequencing and homology-dependent and homology-independent algorithms |journal=Annual Review of Phytopathology |volume=53 |issue= |pages=425–44 |date=2015 |pmid=26047558 |doi=10.1146/annurev-phyto-080614-120030 |url=}}</ref>
Four additional viroids or viroid-like RNA particles were discovered between 2009 and 2015.<ref name="pmid26047558">{{cite journal |vauthors=Wu Q, Ding SW, Zhang Y, Zhu S |title=Identification of viruses and viroids by next-generation sequencing and homology-dependent and homology-independent algorithms |journal=Annual Review of Phytopathology |volume=53 |issue= |pages=425–44 |date=2015 |pmid=26047558 |doi=10.1146/annurev-phyto-080614-120030 |url=}}</ref>

Discovery of new viroids has been difficult without [[next generation sequencing]], but these new techniques are producing significantly better results.<ref name="pmid26047558"/>


In 2014, ''[[New York Times]]'' science writer Carl Zimmer published a popularized piece that mistakenly credited Flores et al. with the hypothesis' original conception.<ref name= Zimmer>{{cite news |last=Zimmer |first=C |author-link=Carl Zimmer |title=A Tiny Emissary From the Ancient Past |url=https://www.nytimes.com/2014/09/25/science/a-tiny-emissary-from-the-ancient-past.html |date=September 25, 2014 |work=[[New York Times]] |access-date=November 22, 2014 }}</ref>
In 2014, ''[[New York Times]]'' science writer Carl Zimmer published a popularized piece that mistakenly credited Flores et al. with the hypothesis' original conception.<ref name= Zimmer>{{cite news |last=Zimmer |first=C |author-link=Carl Zimmer |title=A Tiny Emissary From the Ancient Past |url=https://www.nytimes.com/2014/09/25/science/a-tiny-emissary-from-the-ancient-past.html |date=September 25, 2014 |work=[[New York Times]] |access-date=November 22, 2014 }}</ref>

Revision as of 21:45, 20 January 2022

For a variant of it which is dependent on viruses, see Virusoid.
Viroid
Virus classification Edit this classification
Informal group: Subviral agents
(unranked): Viroid
Families

Pospiviroidae
Avsunviroidae

Viroids are small single-stranded, circular RNAs that are infectious pathogens.[1][2] Unlike viruses, they have no protein coating. All known viroids are inhabitants of angiosperms (flowering plants),[3] and most cause diseases, whose respective economic importance to humans varies widely.

The first discoveries of viroids in the 1970s triggered the historically third major extension of the biosphere—to include smaller lifelike entities —after the discoveries in 1675 by Antonie van Leeuwenhoek (of the "subvisible" microorganisms) and in 1892–1898 by Dmitri Iosifovich Ivanovsky and Martinus Beijerinck (of the "submicroscopic" viruses). The unique properties of viroids have been recognized by the International Committee on Taxonomy of Viruses, in creating a new order of subviral agents.[4]

The first recognized viroid, the pathogenic agent of the potato spindle tuber disease, was discovered, initially molecularly characterized, and named by Theodor Otto Diener, plant pathologist at the U.S Department of Agriculture's Research Center in Beltsville, Maryland, in 1971.[5][6] This viroid is now called potato spindle tuber viroid, abbreviated PSTVd. The Citrus exocortis viroid (CEVd) was discovered soon thereafter, and together understanding of PSTVd and CEVd shaped the concept of the viroid.[7]

Although viroids are composed of nucleic acid, they do not code for any protein.[8][9] The viroid's replication mechanism uses RNA polymerase II, a host cell enzyme normally associated with synthesis of messenger RNA from DNA, which instead catalyzes "rolling circle" synthesis of new RNA using the viroid's RNA as a template. Some viroids are ribozymes, having catalytic properties that allow self-cleavage and ligation of unit-size genomes from larger replication intermediates.[10]

Diener initially hypothesized in 1989 that viroids may represent "living relics" from the widely assumed, ancient, and non-cellular RNA world, and others have followed this conjecture.[11][12] Following the discovery of retrozymes, it is now thought that viroids and other viroid-like elements may derive from this newly found class of retrotransposon.[13][14][15]

The human pathogen hepatitis D virus is a subviral agent similar to a viroid.[16]

Taxonomy

Putative secondary structure of the PSTVd viroid. The highlighted nucleotides are found in most other viroids.

As of 2005:[7]

Lifecycle

The reproduction mechanism of a typical viroid. Leaf contact transmits the viroid. The viroid enters the cell via its plasmodesmata. RNA polymerase II catalyzes rolling-circle synthesis of new viroids.

Viroids only infect plants, and infectious viroids can be transmitted to new plant hosts by aphids, by cross contamination following mechanical damage to plants as a result of horticultural or agricultural practices, or from plant to plant by leaf contact.[17][18] Upon infection, viroids replicate in the nucleus (Pospiviroidae) or chloroplasts (Avsunviroidae) of plant cells in three steps through an RNA-based mechanism. They require RNA polymerase II, a host cell enzyme normally associated with synthesis of messenger RNA from DNA, which instead catalyzes "rolling circle" synthesis of new RNA using the viroid as template.[19][10]

Unlike plant viruses which produce movement proteins, viroids are entirely passive, relying entirely on the host. This is useful in the study of RNA kinetics in plants.[7]

RNA silencing

There has long been uncertainty over how viroids induce symptoms in plants without encoding any protein products within their sequences. Evidence suggests that RNA silencing is involved in the process. First, changes to the viroid genome can dramatically alter its virulence.[20] 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.[21] This 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 contain sequences capable of complementary base pairing with the plant's own messenger RNAs, and induction of degradation or inhibition of translation causes the classic viroid symptoms.[22]

Retroviroids

Retroviroids and retroviroid-like elements are viroids, which are RNA that have a DNA homologue.[23] These entities are thought to be largely exclusive to the carnation, Dianthus caryophyllus, that are closely related to the family of viruses termed 'carnation small viroid-like RNA' (CarSV RNA).[23][24] These elements may act as a homologous substrate upon which recombination may occur and are linked to double-stranded break repair.[24][25] These elements are dubbed retroviroids as the homologous DNA is generated by reverse transcriptase that is encoded by retroviruses.[26][27]

RNA world hypothesis

Diener's 1989 hypothesis[28] had proposed that the unique properties of viroids make them more plausible macromolecules than introns, or other RNAs considered in the past as possible "living relics" of a hypothetical, pre-cellular RNA world. If so, viroids have assumed significance beyond plant virology for evolutionary theory, because their properties make them more plausible candidates than other RNAs to perform crucial steps in the evolution of life from inanimate matter (abiogenesis). Diener's hypothesis was mostly forgotten until 2014, when it was resurrected in a review article by Flores et al.,[26] in which the authors summarized Diener's evidence supporting his hypothesis as:

  1. Viroids' small size, imposed by error-prone replication.
  2. Their high guanine and cytosine content, which increases stability and replication fidelity.
  3. Their circular structure, which assures complete replication without genomic tags.
  4. Existence of structural periodicity, which permits modular assembly into enlarged genomes.
  5. Their lack of protein-coding ability, consistent with a ribosome-free habitat.
  6. Replication mediated in some by ribozymes—the fingerprint of the RNA world.

The presence, in extant cells, of RNAs with molecular properties predicted for RNAs of the RNA world constitutes another powerful argument supporting the RNA world hypothesis. However, the origins of viroids themselves from this RNA world has been cast into doubt by several factors, including the discovery of retrozymes (a family of retrotransposon likely representing their ancestors) and their complete absence from organisms outside of the plants (especially their complete absence from prokaryotes including bacteria and archaea).[13][14][15]

Inspection and quarantine

The development of tests based on ELISA, PCR, and nucleic acid hybridization has allowed for rapid and inexpensive detection of known viroids in biosecurity inspections, phytosanitary inspections, and quarantine. However, the ongoing discovery and evolution of new viroids makes such assays always incomplete.[29]

History

In the 1920s, symptoms of a previously unknown potato disease were noticed in New York and New Jersey fields. Because tubers on affected plants become elongated and misshapen, they named it the potato spindle tuber disease.[30]

The symptoms appeared on plants onto which pieces from affected plants had been budded—indicating that the disease was caused by a transmissible pathogenic agent. A fungus or bacterium could not be found consistently associated with symptom-bearing plants, however, and therefore, it was assumed the disease was caused by a virus. Despite numerous attempts over the years to isolate and purify the assumed virus, using increasingly sophisticated methods, these were unsuccessful when applied to extracts from potato spindle tuber disease-afflicted plants.[6]

In 1971 Theodor O. Diener showed that the agent was not a virus, but a totally unexpected novel type of pathogen, 1/80th the size of typical viruses, for which he proposed the term "viroid".[5] Parallel to agriculture-directed studies, more basic scientific research elucidated many of viroids' physical, chemical, and macromolecular properties. Viroids were shown to consist of short stretches (a few hundred nucleobases) of single-stranded RNA and, unlike viruses, did not have a protein coat. Compared with other infectious plant pathogens, viroids are extremely small in size, ranging from 246 to 467 nucleobases; they thus consist of fewer than 10,000 atoms. In comparison, the genomes of the smallest known viruses capable of causing an infection by themselves are around 2,000 nucleobases long.[31]

In 1976, Sänger et al.[32] presented evidence that potato spindle tuber viroid is a "single-stranded, covalently closed, circular RNA molecule, existing as a highly base-paired rod-like structure"—believed to be the first such molecule described. Circular RNA, unlike linear RNA, forms a covalently closed continuous loop, in which the 3' and 5' ends present in linear RNA molecules have been joined. Sänger et al. also provided evidence for the true circularity of viroids by finding that the RNA could not be phosphorylated at the 5' terminus. In other tests, they failed to find even one free 3' end, which ruled out the possibility of the molecule having two 3' ends. Viroids thus are true circular RNAs.

The single-strandedness and circularity of viroids was confirmed by electron microscopy,[33] The complete nucleotide sequence of potato spindle tuber viroid was determined in 1978.[34] PSTVd was the first pathogen of a eukaryotic organism for which the complete molecular structure has been established. Over thirty plant diseases have since been identified as viroid-, not virus-caused, as had been assumed.[31][35]

Four additional viroids or viroid-like RNA particles were discovered between 2009 and 2015.[29]

In 2014, New York Times science writer Carl Zimmer published a popularized piece that mistakenly credited Flores et al. with the hypothesis' original conception.[36]

See also

References

  1. ^ Navarro, Beatriz; Flores, Ricardo; Di Serio, Francesco (29 September 2021). "Advances in Viroid-Host Interactions". Annual Review of Virology. 8 (1): 305–325. doi:10.1146/annurev-virology-091919-092331. ISSN 2327-056X. PMID 34255541.
  2. ^ "ICTV Report Viroids".
  3. ^ Hadidi A (January 2019). "Next-Generation Sequencing and CRISPR/Cas13 Editing in Viroid Research and Molecular Diagnostics". Viruses. 11 (2): 120. doi:10.3390/v11020120. PMC 6409718. PMID 30699972.
  4. ^ King AM, Adams MJ, Carstens EB, Lefkovitz EJ, et al. (2012). Virus Taxonomy. Ninth Report of the International Committee for Virus Taxonomy. Burlington, MA, USA: Elsevier Academic Press. pp. 1221–1259. ISBN 978-0-12-384685-3.
  5. ^ a b Diener TO (August 1971). "Potato spindle tuber "virus". IV. A replicating, low molecular weight RNA". Virology. 45 (2): 411–28. doi:10.1016/0042-6822(71)90342-4. PMID 5095900.
  6. ^ a b "ARS Research Timeline – Tracking the Elusive Viroid". 2006-03-02. Retrieved 2007-07-18.
  7. ^ a b c Flores R, Hernández C, Martínez de Alba AE, Daròs JA, Di Serio F (2005). "Viroids and viroid-host interactions". Annual Review of Phytopathology. 43: 117–39. doi:10.1146/annurev.phyto.43.040204.140243. PMID 16078879.
  8. ^ Tsagris EM, Martínez de Alba AE, Gozmanova M, Kalantidis K (November 2008). "Viroids". Cellular Microbiology. 10 (11): 2168–79. doi:10.1111/j.1462-5822.2008.01231.x. PMID 18764915. S2CID 221581424.
  9. ^ Flores R, Di Serio F, Hernández C (February 1997). "Viroids: The Noncoding Genomes". Seminars in Virology. 8 (1): 65–73. doi:10.1006/smvy.1997.0107.
  10. ^ a b Daròs JA, Elena SF, Flores R (June 2006). "Viroids: an Ariadne's thread into the RNA labyrinth". EMBO Reports. 7 (6): 593–8. doi:10.1038/sj.embor.7400706. PMC 1479586. PMID 16741503.
  11. ^ Diener TO (December 1989). "Circular RNAs: relics of precellular evolution?". Proceedings of the National Academy of Sciences of the United States of America. 86 (23): 9370–4. Bibcode:1989PNAS...86.9370D. doi:10.1073/pnas.86.23.9370. PMC 298497. PMID 2480600.
  12. ^ Moelling, Karin; Broecker, Felix (2021-03-28). "Viroids and the Origin of Life". International Journal of Molecular Sciences. 22 (7): 3476. doi:10.3390/ijms22073476. ISSN 1422-0067. PMC 8036462. PMID 33800543.
  13. ^ a b Cervera, Amelia; Urbina, Denisse; de la Peña, Marcos (2016-06-23). "Retrozymes are a unique family of non-autonomous retrotransposons with hammerhead ribozymes that propagate in plants through circular RNAs". Genome Biology. 17 (1): 135. doi:10.1186/s13059-016-1002-4. ISSN 1474-760X. PMC 4918200. PMID 27339130.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  14. ^ a b de la Peña, Marcos; Cervera, Amelia (2017-08-03). "Circular RNAs with hammerhead ribozymes encoded in eukaryotic genomes: The enemy at home". RNA Biology. 14 (8): 985–991. doi:10.1080/15476286.2017.1321730. ISSN 1547-6286. PMC 5680766. PMID 28448743.
  15. ^ a b Lee, Benjamin D.; Koonin, Eugene V. (2022-01-12). "Viroids and Viroid-like Circular RNAs: Do They Descend from Primordial Replicators?". Life. 12 (1): 103. doi:10.3390/life12010103. ISSN 2075-1729.
  16. ^ Alves C, Branco C, Cunha C (2013). "Hepatitis delta virus: a peculiar virus". Advances in Virology. 2013: 560105. doi:10.1155/2013/560105. PMC 3807834. PMID 24198831.
  17. ^ a b c d e f g h i j Brian W. J. Mahy, Marc H. V. Van Regenmortel, ed. (2009-10-29). Desk Encyclopedia of Plant and Fungal Virology. Academic Press. pp. 71–81. ISBN 978-0123751485.
  18. ^ De Bokx JA, Piron PG (1981). "Transmission of potato spindle tuber viroid by aphids". Netherlands Journal of Plant Pathology. 87 (2): 31–34. doi:10.1007/bf01976653. S2CID 44660564.
  19. ^ Flores R, Serra P, Minoia S, Di Serio F, Navarro B (2012). "Viroids: from genotype to phenotype just relying on RNA sequence and structural motifs". Frontiers in Microbiology. 3: 217. doi:10.3389/fmicb.2012.00217. PMC 3376415. PMID 22719735.
  20. ^ Hammond RW (April 1992). "Analysis of the virulence modulating region of potato spindle tuber viroid (PSTVd) by site-directed mutagenesis". Virology. 187 (2): 654–62. doi:10.1016/0042-6822(92)90468-5. PMID 1546460.
  21. ^ Wang MB, Bian XY, Wu LM, Liu LX, Smith NA, Isenegger D, et al. (March 2004). "On the role of RNA silencing in the pathogenicity and evolution of viroids and viral satellites". Proceedings of the National Academy of Sciences of the United States of America. 101 (9): 3275–80. Bibcode:2004PNAS..101.3275W. doi:10.1073/pnas.0400104101. PMC 365780. PMID 14978267.
  22. ^ Pallas V, Martinez G, Gomez G (2012). "The interaction between plant viroid-induced symptoms and RNA silencing". Antiviral Resistance in Plants. Methods in Molecular Biology. Vol. 894. pp. 323–43. doi:10.1007/978-1-61779-882-5_22. hdl:10261/74632. ISBN 978-1-61779-881-8. PMID 22678590.
  23. ^ a b Daròs J A, Flores R (1995). "Identification of a retroviroid-like element from plants". Proceedings of the National Academy of Sciences of the United States of America. 92 (15): 6856–6860. Bibcode:1995PNAS...92.6856D. doi:10.1073/pnas.92.15.6856. PMC 41428. PMID 7542779.
  24. ^ a b Hegedűs K, Dallmann G, Balázs E (2004). "The DNA form of a retroviroid-like element is involved in recombination events with itself and with the plant genome". Virology. 325 (2): 277–286. doi:10.1016/j.virol.2004.04.035. PMID 15246267.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  25. ^ Truong LN, Li Y, Shi LZ, Hwang PY, He J, Wang H, et al. (May 2013). "Microhomology-mediated End Joining and Homologous Recombination share the initial end resection step to repair DNA double-strand breaks in mammalian cells". Proceedings of the National Academy of Sciences of the United States of America. 110 (19): 7720–25. Bibcode:2013PNAS..110.7720T. doi:10.1073/pnas.1213431110. PMC 3651503. PMID 23610439.
  26. ^ a b Flores R, Gago-Zachert S, Serra P, Sanjuán R, Elena SF (June 18, 2014). "Viroids: survivors from the RNA world?" (PDF). Annual Review of Microbiology. 68: 395–414. doi:10.1146/annurev-micro-091313-103416. hdl:10261/107724. PMID 25002087.
  27. ^ Hull R (October 2013). "Chapter 5: Agents Resembling or Altering Virus Diseases". Plant virology (Fifth ed.). London, UK: Academic Press. ISBN 978-0-12-384872-7.
  28. ^ Diener, T O. "Circular RNAs: relics of precellular evolution?."Proc.Natl.Acad.Sci.USA, 1989;86(23):9370-9374
  29. ^ a b Wu Q, Ding SW, Zhang Y, Zhu S (2015). "Identification of viruses and viroids by next-generation sequencing and homology-dependent and homology-independent algorithms". Annual Review of Phytopathology. 53: 425–44. doi:10.1146/annurev-phyto-080614-120030. PMID 26047558.
  30. ^ Owens RA, Verhoeven JT (2009). "Potato Spindle Tuber". Plant Health Instructor. doi:10.1094/PHI-I-2009-0804-01.
  31. ^ a b Pommerville, Jeffrey C (2014). Fundamentals of Microbiology. Burlington, MA: Jones and Bartlett Learning. p. 482. ISBN 978-1-284-03968-9.
  32. ^ Sanger HL, Klotz G, Riesner D, Gross HJ, Kleinschmidt AK (November 1976). "Viroids are single-stranded covalently closed circular RNA molecules existing as highly base-paired rod-like structures". Proceedings of the National Academy of Sciences of the United States of America. 73 (11): 3852–6. Bibcode:1976PNAS...73.3852S. doi:10.1073/pnas.73.11.3852. PMC 431239. PMID 1069269.
  33. ^ Sogo JM, Koller T, Diener TO (September 1973). "Potato spindle tuber viroid. X. Visualization and size determination by electron microscopy". Virology. 55 (1): 70–80. doi:10.1016/s0042-6822(73)81009-8. PMID 4728831.
  34. ^ Gross HJ, Domdey H, Lossow C, Jank P, Raba M, Alberty H, Sänger HL (May 1978). "Nucleotide sequence and secondary structure of potato spindle tuber viroid". Nature. 273 (5659): 203–8. Bibcode:1978Natur.273..203G. doi:10.1038/273203a0. PMID 643081. S2CID 19398777.
  35. ^ Hammond RW, Owens RA (2006). "Viroids: New and Continuing Risks for Horticultural and Agricultural Crops". APSnet Feature Articles. doi:10.1094/APSnetFeature-2006-1106.
  36. ^ Zimmer, C (September 25, 2014). "A Tiny Emissary From the Ancient Past". New York Times. Retrieved November 22, 2014.
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