Biological Sciences
Viroid
Viroids are small, single-stranded, circular RNA molecules that are infectious and can cause disease in plants. Unlike viruses, viroids do not encode any proteins and rely on host cellular machinery for replication. They are known for their ability to disrupt normal plant growth and development, making them a significant concern in agriculture and horticulture.
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11 Key excerpts on "Viroid"
eBook - ePubPlant Viruses
Volume I: Structure and Replication
- C.L. Mandahar(Author)
- 2018(Publication Date)
- CRC Press(Publisher)
Chapter 8 Plant Viroids: A Biochemical NoveltyR. P. SinghTable of Contents
I. Introduction II. Viroid Diseases A. Pathological Significance B. Discovery of Viroid Nature C. The Viroid Diseases Reported to Date D. Origin of Viroid Diseases E. Transmission and Spread of Viroid Diseases F. Viroid Isolation and Maintenance G. Viroid Detection by Biochemical Methods III. Biophysical Nature of Viroids A. Purification B. Infectivity of Linear and Circular Viroid Molecules C. Electron Micrograph of Viroid Molecules D. RNA Sequencing — Methods E. Primary Structure and Viroid Groups F. RNA Sequence Variability of Viroid Isolates G. RNA Sequences — Secondary and Tertiary Structures H. Structural Transitions of Viroid Molecules I. In Vivo Structures of Viroids IV. Replication A. Absence of Translational Products B. Existence of Oligomeric Complementary RNAs C. Enzymes Involved in Viroid Replication D. Nonenzymatic Cleavage of Oligomers E. Models of Replication F. Replication Sites V. Pathogenicity A. Nucleotide Sequence Comparison of Variant Isolates B. Infectivity of cDNA and RNA Transcripts C. Site-Specific Mutations in cDNAs D. Infectivity of Viroid cDNA Chimeras VI. Speculations on the Possible Origin of Viroids A. Presequence Hypotheses — A Historical Preview B. The Present-Day Concept — The Intron Connection Acknowledgments References I. Introduction
Viroids are low-molecular weight1 , 2 covalently closed circular RNA3 molecules that can cause economically important diseases of higher plants.4 - 6 Viroids are distinguished from viruses by the absence of a protein coat, lack of mRNA activity, and by the homogenous structure, structural transitions, and hydrodynamic behavior of their RNA molecules.7 - 10 If one could rephrase the expression "small is beautiful" to include "complex and mysterious" that would describe the Viroids.II. Viroid Diseases
eBook - ePub- Roger Hull(Author)
- 2001(Publication Date)
- Academic Press(Publisher)
CHAPTER 14Viroids, Satellite Viruses and Satellite RNAs
There are various small RNAs associated with plant pathogenic situations. Essentially, most fall into two groups: those that can replicate autonomously and those that require a functional virus for their replication. The former group is termed Viroids and the latter include satellites and defective nucleic acids. Defective nucleic acids are described in Chapter 8 (Section IX.C ). In this chapter, I will describe Viroids and satellites.I. ViroidS
Various important virus-like diseases in plants have been shown to be caused by pathogenic RNAs known as Viroids, a term first introduced by Diener (1971) to describe the infectious agent causing the spindle tuber disease of potato. They are small circular molecules, a few hundred nucleotides long, with a high degree of secondary structure. They do not code for any polypeptides and replicate independently of any associated plant virus. Viroids are of practical importance as the cause of several economically significant diseases and are of general biological interest as being among the smallest known agents of infectious disease. Work on Viroids has been reviewed many times, for example by Diener (1987b) , Diener (1993) ,Flores et al. (1997), Symons (1997) and Diener (1999) . The most studied Viroid is potato spindle tuber Viroid (PSTVd). Viroid names are abbreviated to initials with a ‘d’ added to distinguish them from abbreviations for virus names. Acronyms for Viroids are listed in Appendix 1
- Donald D Bills, Shain-dow Kung(Authors)
- 1995(Publication Date)
- World Scientific(Publisher)
Introduction Viroids are the smallest known agents of infectious disease. They are responsibl e for a number of economical ly significant disea ses in 201 202 vegetatively propagated crops, and much effort has been devote d to their molecular characte rization in h o p es of understanding how these u n u s u al pa th og ens interact with their hosts to cause disease (Diener, 1987). Vi r o id s are characte rized as being autonomously replicating, circula r, s ingl e -str an d e d RNA's w h ic h range in size from 246 to 375 nucleotides. T he y lack b o th th e p r o te i n coat characteris tic of viruses and any detectable messenger RNA activity. In a su sceptibl e plant host, they can re pli c a te to levels of up to 10,000 copies per cell (Schumacher et al., 1983). In m an y case s, Viroid replication is accompanied by the production of symptoms in the host; in other cases, Viroid replication can lead to the accumul ation of considerable Viroid concentrations without the p r odu cti o n of noticeabl e disea se symptoms. The complexity of the interact ion of the Viroid with it s host has been made apparent from results o f numerous studies which have been car ried out in several laboratories in order to understand and elucidate the mechanisms of Viroid p atho g e n esis. In our laboratory, mutational analysis of potato spindle tuber (PST V d) and tomato apical stunt viro ids (TASVd) has al l ow e d us to genetic ally isolate such normally inter related processes as re pli cation, cel l-to -cel l movement, and disease induction. In addition, the c o n s truct io n of novel interspecific chimeric viro id molecules between T A S V d and citrus exocortis viro id (CEVd) has al lowed us to determine the contribution of individual st ruc t ur al domains to Viroid pathogenic ity.
eBook - PDF- Irwin Rubenstein, Ronald L. Phillips, Charles E. Green, Irwin Rubenstein, Ronald L. Phillips, Charles E. Green(Authors)
- 2013(Publication Date)
- Academic Press(Publisher)
Aside from the lack of a protein coat and the smallness of their genomes, Viroids differ from viruses in that infection with Viroids apparently does not lead to the synthesis of novel, pathogen-specific proteins. Also, PSTV is the first known RNA pathogen of plants which pos-sesses complementarity to its host DNA. Having these properties, Viroids lend themselves admirably to studies, on the molecular level, of the mechanisms of pathogenesis and control of gene regulation in eucaryotic cells. From a practical standpoint it can be predicted that many infectious diseases of plants and possibly of animals, the etiol-ogy of which is now obscure, will be found to be caused by agents similar to presently known Viroids. Some of these plant diseases may be of considerable economic importance. A case in point is cadang-cadang disease of coconut palms, which poses a serious threat to the coconut industry, particularly in the Philippines. Although information is incomplete, recent results demonstrated the association of a Viroid-like, low-molecular-weight RNA with extracts from diseased tissue and its absence in extracts from healthy tissue, suggesting that cadang-cadang disease may be of Viroid etiology (Randies, 1975). Methods developed for the study and purification of Viroids have already been adapted as a valuable diagnostic aid for index-ing elite or basic potato seed stocks in certification programs (Morris and Wright, 1975). SUMMARY The spindle tuber disease of potato, which was previously 286 T. O. Diener believed to be of viral etiology, has been shown to be caused by a free infectious RNA of low molecular weight (about 8 x 10^). This agent is the first representative of a newly recognized class of pathogens, the Viroids, which have been characterized by the absence of a dormant phase (virions) and by genomes that are much smaller than those of known viruses.
eBook - PDF- Shain-dow Kung, Shang-fa Yang(Authors)
- 1998(Publication Date)
- World Scientific(Publisher)
Chapter 13 The Discovery of the Viroid 1 Theodor O. Diener Center for Agricultural Biotechnology and Department of Plant Biology University of Maryland, College Park, MD 20742, USA ABSTRACT The unexpected discovery of the Viroid in 1971 has led to the recognition that pathogens much smaller than the smallest viruses exist and that, despite their very limited genetic information, such subviral agents can cause devastating diseases. Although, initially, opinion as to the Viroid's proper classification varied widely, with the elucidation of its unusual molecular structure, its lack of mRNA activity, and its autonomous replication, it has become increasingly evident, that the Viroid represents an entirely novel type of pathogen, clearly distinct from all viruses. Here, I chronologically document the events that have led to its discovery. Preludes to Viroid Discovery Recognition of the fundamental disparity between viruses and Viroids became possible only after certain basic principles of virology and molecular biology had been established. These principles helped create an intellectual milieu in which the existence of free nucleic acid pathogens could not a priori be ruled out. Aside from general biological principles, at least four important prerequisites can be identified: (i) Foremost was the realization that the genetic information of viruses resides in their nucleic acid component, a fact that, in the case of plant viruses, was most dramatically established with the ^ i s presentation is an extended and modified version of a paper entitled Portraits of Viruses: the Viroid, (Intervirology 22,1-16,1984), published by S. Karger A.G., Basel, Switzerland. 203
eBook - PDFViruses
Agents of Evolutionary Invention
- Michael G. Cordingley(Author)
- 2017(Publication Date)
- Harvard University Press(Publisher)
Soon it was visualized under the electron microscope; mixed with bacterio-phage T7 DNA, it was but a speck on the image of the vast intertwining bacteriophage genome. This class of infectious agents, considered sub-viral in nature, were christened Viroids . In 1978 PSTV would become the first eukaryotic pathogen to be sequenced in full. We might then consider that the discovery of Viroids represented a watershed and ushered in the era of genomics. Today more than thirty species of Viroids have been described, belonging to two distinct families (Flores et al. 2014; Tsagris et al. 2008; Tabler and Tsagris 2004; Flores et al. 2005; Daros, Elena, and Flores 2006). They infect a variety of other plant species, among them economi-cally important crops such as citrus trees, eggplant, coconut, and avocado, as well as ornamentals such as chrysanthemums and coleus. They have in common a single-stranded RNA genome between 246 and 401 nucleo-tides in length, some ten times smaller than the smallest bacteriophage genome. The genome is circular, and its compact folded nature is attributed to extensive self-complementarity of the nucleotide sequence leading to base pairing and complex secondary structures. The most remarkable aspect of Viroids is that their genetic material encodes no proteins, yet they can orchestrate efficient autonomous replication and transmission between cells and even between plants. Belying their apparent simplicity, they have evolved to rely exclusively on host cell proteins to support their lifestyles. They are a compelling illustration that the ability to confer phenotype is not the exclusive domain of proteins. Traditionally we think of protein function as the ultimate arbiter of phenotype, but Viroids remind us that nucleic acid sequences themselves can definitively be functional and confer
eBook - PDF- Esteban Domingo, Robert G. Webster, John F. Holland(Authors)
- 1999(Publication Date)
- Academic Press(Publisher)
Viroids as a class of pathogenic RNA owe their recognition as an unusual molecular species to the expression of biological activity in the form of plant disease symptoms. In addi- tion, most new Viroids are described as a result of some disease expression in crop plants. These undesirable plant responses are, however, cou- pled with the existence of symptomless carrier plant species for numerous Viroids. Thus, with- in the host range of any one Viroid species there exists a selection process for parasitism or com- mensalism in the accommodation of specific quasi-species. This selection can undoubtedly be influenced by other factors, such as environment and host genome variations. Thus, replication and reten- tion of Viroids can occur in the absence of any obvious pathogenic response. This relationship among quasi-species and host interactions are represented in the distribution of quasi-species (Figure 3.1). The distinction in the sequences of Viroids inducing disease symptoms or simply replication and retention can be in the range of a few to a single nucleotide as for CEVd (Semancik et al, 1993; Fagoaga et al., 1995; Fagoaga and Duran-Vila, 1996) and PSTVd (Wassenegger et al., 1996) respectively. Less frequently have the positive effects of Viroids on the performance and survival of the host been emphasized. The association with dis- ease as well as the virus-like nature implied by the term Viroid has fostered the principle of production of Viroid-tested plant materials in plant protection programs throughout the world. The implicit guiding philosophy fostered by these agencies considers Viroid-free plants to be a means of providing disease control and superior agricultural return. Although valid for most cases involving Viroids inducing diseases, as a result of the certification programs aiming at the control of plant diseases, growers may
- Karl Maramorosch(Author)
- 2012(Publication Date)
- Academic Press(Publisher)
The presence of such RNA species would suggest that the host components required for Viroid replication are not limited to plant cells. With regard to the second question (concerning disease agents), the recent evidence obtained by Coggin and co-workers (1981, 1983) linking a Viroid-like agent to an epide-mic of infectious lymphoma in hamsters is highly suggestive. With this finding in mind, it would also seem prudent to apply the techniques of Viroid detection to other diseases of unknown etiology, of which acquired immune deficiency syn-drome [AIDS (Curran, 1983; Harris et al., 1983)], has served as an example. In the initial stages of investigation, several lines of evidence have suggested that a search for an AIDS-specific Viroid might be fruitful. First, although a number of fami-liar viruses were identified in AIDS patients, no AIDS-speci-fic micro-organism (viral or bacterial) was identified in initial screening studies, despite extensive examination of tissues from affected individuals. Viroids do not form particles (Diener, 1979). Thus, a Viroid-like agent associa-ted with any disease would escape detection in all of the usual assays employed to identify conventional viruses. Second, Viroids cause elaborations of cellular membranes (Semancik and Vanderwoude, 1976; Sänger 1982) which could be compared to the vesicular rosettes recently described in lymphoid cells of AIDS patients (Ewing et al., 1983). Third, the agent studied by Coggin and co-workers (1981, 1983) was shown to affect cells of the immune system—the target for AIDS. Fourth, like AIDS, Viroid diseases are known to arise suddenly and spread rapidly, often with disastrous consequen-ces for the host (Hollings and Stone, 1970; Randies, 1975).
eBook - PDF- Abraham Marcus(Author)
- 1989(Publication Date)
- Academic Press(Publisher)
A possible clue to explain the mechanism of Viroid pathogenesis may be the recent discovery that an M r 68K host protein is differentially phosphory-lated in extracts from Viroid-infected and mock-inoculated tissues. This phosphoprotein is immunologically related to a double-stranded RNA-dependent protein kinase from virus-infected, interferon-treated human cells (Hiddinga et al., 1988). These findings suggest, but do not prove, that this protein, which is similar to double-stranded RN A-dependent protein kinases implicated in mammalian systems in the regulation of protein synthesis and virus replication, is involved in both plant virus and Viroid pathogenesis. If so, plant viruses and Viroids would affect similar host systems and thus explain the similarity of Viroid- and virus-induced symptoms in plants. Viroids 559 VIII. POSSIBLE Viroid ORIGINS At the time when the Viroid concept was initially advanced (Diener, 1971b), Viroids could be regarded as either very primitive or degenerate relatives of conventional viruses. Knowledge accumulated since then and summarized in this chapter has rendered this concept increasingly less likely. The lack of mRNA activity and novel molecular structure (see Sec-tions IV,B and V,C) imply a far greater phylogenetic distance from viruses than could be previously imagined. Comparative sequence analysis of five related Viroids (PSTV, CEV, CSV, TASV, and TPMV) has revealed striking similarities with the ends of trans-posable genetic elements (Kiefer et al., 1983). The presence of inverted repeats often ending with U-G and C-A and flanking imperfect direct repeats suggests that Viroids may have originated from transposable elements or retroviral proviruses by deletion of interior sequences. Alternatively, these similarities between Viroids and transposable genetic elements could be a consequence of convergent evolution.
eBook - PDFPlant Disease: An Advanced Treatise
How Pathogens Induce Disease
- James G. Horsfall(Author)
- 2012(Publication Date)
- Academic Press(Publisher)
Depend-ing on the virus, the viral RNAs may be either single- or double-stranded. In many cases the total viral genome is divided among several RNA molecules, which may be encapsidated in separate nucleoprotein par-ticles. Furthermore, in infected host cells, small RNAs may be found which are specific pieces of the full-sized parental viral RNAs; some of these RNAs serve as monocistronic messenger RNAs for the viral-coded polypeptides (Beachy and Zaitlin, 1977). As would be expected, DNA plant viruses also generate RNA molecules in the infected cell (Howell and Hull, 1978). In many cases, virions also contain trace amounts of metals; certain ones may contain lipids, carbohydrates, polyamines, transfer RNAs, and even host proteins. B. Viroids In contrast to viruses, Viroids appear to have only three possible products that could be the initiators of disease, namely, (1) the small Viroid RNA itself, which may be either linear or circular, ( 2 ) its recently discovered complementary strand (Grill and Semancik, 1978), and possibly (3) a double-stranded form consisting of the Viroid hydrogen-bonded to its complement. Comprehensive investigations have not un-covered any coat protein or translational product of Viroid RNAs; they apparently do not contain genetic information that codes for protein (reviewed in Diener and Hadidi, 1977 ). V I . W H I C H P R O D U C T S A R E I N V O L V E D ? Specific information as to the possible involvement of all the virus or Viroid products in disease is not available, but at least three groups can be eliminated as having a primary role in disease on largely cir-cumstantial grounds. 264 MILTON ZAITLIN A. Virus Replication It is generally conceded that the symptoms induced by a virus are not due to the direct effect of the stress put on the host by being forced to synthesize extra protein and nucleic acid, although it is possible that in specialized cases such stress might affect a plant adversely.
eBook - ePubViroids
Properties, Detection, Diseases and their Control
- Ahmed Hadidi, Ricardo Flores, John W. Randles, Joseph S. Semancik, John Randles, Joseph Semancik(Authors)
- 2003(Publication Date)
- CSIRO PUBLISHING(Publisher)
On this basis, it was thought that their pathogenicity had to be exerted through direct interference with some critical cellular targets (Diener 1979 ; Semancik and Conejero 1987 ; Conejero et al. 1979). From this, and taking into account the replication and location of most Viroids in the nucleus (Riesner 1987 ; Robertson and Branch 1987 ; Sänger 1987), the obvious strategy was to look for possible interference of Viroid RNA molecules or their complementary replicative forms, with either host nucleic acids or proteins, as the primary pathogenic event. Thus, it was suggested that Viroids express their pathogenicity by altered regulation of gene expression (Rackwitz et al. 1981 ; Diener 1981 ; Dickson 1981 ; Solymosy and Kiss 1985) and altered translocation of proteins through base pairing with RNA signal recognition particles (Haas et al. 1988). These interpretations were supported by theoretical considerations. A different type of approach in our laboratory (Conejero and Granell 1986) led to evidence indicating that Viroids seem to be elicitors of a general response system of the host plant (Conejero et al. 1990). Very soon after the discovery of Viroids, any new finding or idea concerning the role of RNA in any of the steps of gene expression (transcription, RNA maturation, translation) and/or their regulation, has been used to help interpretation of Viroid pathogenicity. In the last decade the emergence of the new concept of gene silencing (GS), and its specific signaling by small RNA molecules, again could help to understand how Viroids produce developmental distortions and/or the plants defend themselves, specifically, against the systemic infection of Viroids
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