Viroids are small single-stranded circular RNAs that infect plants (Flores et al. , 2004). These subviral pathogens are characterized by complementary base pairs and long secondary structures. Their genome is approximately 400 nucleotidees in length. RNA viriods do not result in any protein hence they are called unencapsulated, but they multiply by themselves without the help of any other viruses. Their replication takes place in the infected cells. Satellite viruses are typically similar to viroids but these RNA viruses are situated within the protein coat or capsids of specific helper viruses.
Such parasitic locations of satellite viruses are necessary for them to replicate. A prime example of a satellite virus is the human hepatitis ? virus (HDV) which is dependent of the hepatitis B virus for the packaging and spreading of the HDV to other organisms (Taylor, 2003). The RNA of the human hepatitis ? virus is composed of a viroidlike domain, which is a segment that shows remarkable similarities to viroids and satellite viruses. Viroids and satellite viruses replicated through the employment of oligomeric RNA intermediates that undergo the rolling circle scheme of DNA replication.
The genome of the HDV is composed of a tiny single-stranded circular negative sense RNA of approximately 1,700 nucleotides in length. Within the genome, self-cleaving motifs such as the delta ribozymes and an open reading frame are located and these code for two viral proteins. There are several hypotheses that have been suggested to elucidate the evolution and origin of viroids. One of the theories suggested that viroids probably came from retroviruses or transposable elements that have lost their interior sequences.
Such scenario would translate into the concept that viroids are introns or non-coding gene segments that escaped from another virus. Another theories on the evolution and origin of viroids describes that they are an advanced for or antenna or signal RNAs which eukaryotic cells considered as unreactive. The discovery of viroids and satellite viruses thus supports the concept that RNA existed first before DNA. The feature of certain RNAs having catalytic or reactive domain also supports the notion that RNA preceded DNA in terms of evolution.
Several investigations have also described primitive types of RNA molecules that showed catalytic properties which are considered as evolutionary relics of the earlier existing RNA world. In addition, the idea that a common ancestor to viroids and satellite viruses must have existed is also unquestionable, due to the fact that there are significant similarities between their sequences and catalytic domains. Such monophyletic origin of viroids and viroidlike satellite RNAs are thus a very interesting topic for research and investigation.
Viroids are categorized into two families according to the presence or absence of conserved regions, hammerhead ribozymes and their location in within the cell. There are two common areas wherein viroids are typically situated. They are either found in the nucleus or in the chloroplast. Satellite viruses, on the other hand, are further categorized into three groups. The large satellite viruses generate proteins, while the small linear satellite viruses and the circular satellite viruses do not code for proteins.
Since the genomes of viroids and viroid-like satellite RNAs have no coding properties and the HDV carries a highly restricted coding capability, it has been generally accepted that these entities are mosaics of functional RNA motifs providing specific activities such as ribozymes and signals for recruiting and activating host proteins such as the RY motif. Comprehensive molecular investigations in the field of virology have resulted in priceless information on the sequence of their genomes.
Such efforts would provide more information and lead to a better understanding of these subviral agents as well as their sequence motifs. The potato spindle tuber and at least 15 other crop diseases were the first species that were reported to be infect by viroids. In 1971, Theodor O. Diener, a plant pathologist, coined the word viroid because of their features which were very much like a virus (Simon et al. , 2004). That potato spindle tuber viroid was characterized to be of 130,000 daltons in size.
Other known viroids that are classified as Group A viroids include the avocado sunblotch viroid, the peach latent mosaic viroid. These viroids follow the symmetric rolling circle mechanism for genome replication. This involves the replication of the negative RNA strand and then cut by a ribozyme. The RNA then reorients itself into a circular shaped negative circle. Another rolling circle step generates a long positive strand which is then cut up by the ribozyme. This shorter viroid RNA segment is then pasted together through ligation into a circular form.
Another group of viroids termed as Group B viroids include the coconut cadang-cadang viroid, the tomato plant machoviroid. These viroids on the other hand follow the asymmetric mechanism of genome replication. This involves the positive infecting circular RNA strand serving as a template for replication, resulting in a large linear multimeric negative strand. It has been suggested the RNA polymerase III facilitates this type of genome replication. These viroids employ an asymmetric mode of genome replication and then generate a positive RNA strand from that linear nucleic acid.
A host RNAse activity then cut the positive strand into several units of standard viroid length. These fragments are then put together through the process of ligation to create a circular viroid. A subgroup of viroids includes the citrus bent leaf viroid and the pear blister canker viroid. Group A viroids lack a central conserved region (CCR) and possess a ribozyme activity. Additionally, it is speculated that Group A viroids may replicate in chloroplasts whereas Group B viroids replicate in the nucleus and nucleolus.
Three enzymatic activities are required for viroid replication, an RNA polymerase, RNAse and an RNA ligase. Probably there is more than one mechanism responsible for viroid pathogenesis. Recent evidence suggests that one pathway is due to viroid RNA activating a plant RNA activated protein kinase, or PKR, which is analogous to the PKR enzyme activated by viral RNAs in mammalian cells. Protein synthesis is inhibited and this causes pathogenic effects. In the case of potato spindle tuber viroid, there is a good correlation between a strain’s pathogenicity and its ability to activate PKR in vitro.