Viroids and Prions

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  • Topic: Prion, RNA, Transmissible spongiform encephalopathy
  • Pages : 14 (4574 words )
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  • Published : February 16, 2012
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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.[1] The smallest discovered is a 220 nucleobase scRNA (small cytoplasmic RNA) associated with the rice yellow mottle sobemovirus (RYMV).[2] In comparison, the genome of the smallest known viruses capable of causing an infection by themselves are around 2kilobases in size. The human pathogen hepatitis D is similar to viroids.[3] Viroids are extremely small in size, consisting of less than 10,000 atoms.[4] Viroids were discovered and given this name by Theodor Otto Diener, a plant pathologist at the Agricultural Research Service in Maryland, in 1971.[5][6][7] Viroid RNA does not code for any protein.[8] The replication mechanism involves RNA polymerase II, an 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 template. Some viroids are ribozymes, having catalytic properties which allow self-cleavage and ligation of unit-size genomes from larger replication intermediates.[9] The first viroid to be identified was the potato spindle tuber viroid (PSTVd). Some 33 species have been identified. -------------------------------------------------

* Family Pospiviroidae
* Genus Pospiviroid; type species: Potato spindle tuber viroid * Genus Hostuviroid; type species: Hop stunt viroid
* Genus Cocadviroid; type species: Coconut cadang-cadang viroid * Genus Apscaviroid; type species: Apple scar skin viroid * Genus Coleviroid; type species: Coleus blumei viroid 1 * Family Avsunviroidae

* Genus Avsunviroid; type species: Avocado sunblotch viroid * Genus Pelamoviroid; type species: Peach latent mosaic viroid * Genus Elaviroid; type species: Eggplant latent viroid -------------------------------------------------

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 thatRNA silencing is involved in the process. First, changes to the viroid genome can dramatically alter its virulence.[10] This reflects the fact that any siRNAs produced would have less complementary base pairing with target messenger RNA. Secondly, siRNAscorresponding to sequences from viroid genomes have been isolated from infected plants.[11] Finally, transgenic expression of the noninfectious hpRNA of potato spindle tuber viroid develops all the corresponding viroid like symptoms.[12] 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 theRNA-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.

Virus classification is the process of naming viruses and placing them into a taxonomicsystem. Similar to the classification systems used for cellular organisms, virus classification is the subject of ongoing debate and proposals. This is mainly due to the pseudo-livingnature of viruses, which are not yet definitively classified as living or non-living. As such, they do not fit neatly into the established biological classification system in place for cellular organisms. Viruses are mainly classified by phenotypic characteristics, such as morphology, nucleic acid type, mode of replication, host organisms, and the type of disease they cause. Currently there are two main schemes used for the classification of viruses: the ICTV system and Baltimore classification system, which places viruses into one of seven groups. Accompanying this broad method of classification are...
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