Tomato bushy stunt virus

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Tomato bushy stunt virus
2tbv capsid ray.png
The capsid of the tomato bushy stunt virus, with the three symmetrically distinct coat protein (p41) monomers colored in orange, green, and blue. [1]
Virus classification Red Pencil Icon.png
(unranked): Virus
Realm: Riboviria
Kingdom: Orthornavirae
Phylum: Kitrinoviricota
Class: Tolucaviricetes
Order: Tolivirales
Family: Tombusviridae
Genus: Tombusvirus
Species:
Tomato bushy stunt virus

Tomato bushy stunt virus (TBSV) is a virus of the tombusvirus family. [2] It was first reported in tomatoes in 1935 and primarily affects vegetable crops, though it is not generally considered an economically significant plant pathogen. Depending upon the host, TBSV causes stunting of growth, leaf mottling, and deformed or absent fruit. The virus is likely to be soil-borne in the natural setting, but can also transmitted mechanically, for example through contaminated cutting tools. TBSV has been used as a model system in virology research on the life cycle of plant viruses, particularly in experimental infections of the model host plant Nicotiana benthamiana . [3] [4]

Contents

Host range

N. benthamiana, a common experimental host for TBSV. Nicotiana benthamiana plant.jpg
N. benthamiana, a common experimental host for TBSV.

TBSV has a broad host range under experimental conditions and has been reported to infect over 120 plant species spanning 20 families. However, under natural conditions its range is much narrower and generally comprises crop vegetables and ornamental plants. It was first identified in tomato plants and also has been documented to affect apple, artichoke, cherry, grapevine, hops, and pepper. Although it causes significant loss of yield in tomato plants, it is not considered an economically significant pathogen. [4] [5] It is, however, a very well-established model system for the study of plant viruses, usually through experimental infection of Nicotiana benthamiana or Nicotiana clevelandii , relatives of tobacco plants in which TBSV can cause systemic infection. Notably, the common model plant Arabidopsis thaliana is not a host. [3] [4] TBSV can also replicate in yeast in laboratory conditions. [6]

Signs

The signs of TBSV are host-dependent. Local infections can cause necrotic or chlorotic lesions. Systemic infections can cause stunted growth, deformed or absent fruit, and damaged leaves; in agricultural settings yield can be significantly reduced. The stunted, "bushy" appearance of the tomato plants in which the virus was first discovered gave the pathogen its name. In some hosts, most notably N. benthamiana , TBSV can cause lethal systemic necrosis. [4] [5]

Transmission

TBSV is thought to be passively transmitted in the wild, primarily through soil or water. There are no known vector organisms; transmission by aphids, mites, and the fungus Olpidium brassicae has specifically been ruled out. [5] However, the closely related tombusvirus Cucumber necrosis virus (CNV) has been observed to be transmitted by Olpidium bornovanus zoospores, so transmission of TBSV by as-yet unknown vector remains a possibility. [4] TBSV can also be transmitted through seed or by mechanical inoculation. [4] [5] In experimental tests, the virus can survive passage through the human digestive system if consumed in food and will remain infectious; it has been hypothesized that spread through sewage could occur. [7]

Distribution and management

TBSV is distributed fairly widely across central and western Europe, north Africa, and North and South America. [4] [5] No specific control measures are recommended for the virus, though pest management guidelines distributed by the University of California recommend avoiding fields with a history of TBSV or using long crop rotations. [8]

Taxonomy

TBSV is assigned to the Tombusvirus genus in the family Tombusviridae . [9] Both the genus and the family derive their names from an abbreviation of "tomato bushy stunt virus". [10]

Structure

Schematic drawings of a Tombusviridae virion (cross-section and side view) Tombusviridae virion.jpg
Schematic drawings of a Tombusviridae virion (cross-section and side view)

TBSV is an unenveloped icosahedral virus with a T=3 viral capsid composed of 180 subunits of a single capsid protein. Its structure was studied extensively by X-ray crystallography from the late 1950s; its icosahedral symmetry was first identified by structural biologist Donald Caspar, who also pioneered the study of the tobacco mosaic virus. [11] A near-atomic-resolution map was obtained in 1978 by a research team including Stephen C. Harrison. [12] [13]

Genome and protein complement

Tombusvirus genome map Tombusvirus genome.png
Tombusvirus genome map

TBSV is a positive-sense single-stranded RNA virus with a linear genome of ~4800 nucleotides. [14] [15] The genome contains five genes that encode a replicase composed of two proteins (p33 and p92), a capsid protein (called CP or p41), and two additional proteins, the RNA silencing suppressor p19 and movement protein p22. [4] These two proteins are expressed from overlapping genes arranged so that the open reading frame of p19 is completely within the ORF of p22. [16] The genome contains one additional possible gene, called pX, of unknown function. [4]

p33 and p92

Together p33 and p92 comprise the viral replicase complex. P33 is smaller and p92 is produced through ribosomal read-through of the p33 stop codon, resulting in a shared N-terminal amino acid sequence and a large excess of p33 relative to p92. P33 proteins cooperatively bind single-stranded nucleic acids, while the p92 protein is a RNA-dependent RNA polymerase (RdRp). Both are essential to viral proliferation. Both proteins are associated with cell membranes. [4]

p41 (capsid protein)

The viral capsid protein CP, or p41, is a double jelly roll protein that assembles into an icosahedral capsid containing 180 copies of the protein. Formation of virions is not always necessary for localized spread of the virus into neighboring plant cells, because ribonucleoprotein particles containing viral genetic material can spread to immediate neighbors through plasmodesmata. However, the capsid protein is required for systemic infection. [4]

p19

The p19 protein in complex with double-stranded RNA. 1R9F tombusvirus p19.png
The p19 protein in complex with double-stranded RNA.

The p19 protein is a pathogenicity factor and functions by suppressing the RNA silencing pathway, a common form of antiviral defense. The p19 protein binds short interfering RNAs and prevents their incorporation into the RNA-induced silencing complex (RISC), thereby allowing viral propagation in the host plant. [3] [17] [18] The presence of p19 is necessary for systemic infection or for lethal infection in some hosts; in the experimental host N. benthamiana , p19 largely mediates the lethal systemic necrosis that is the outcome of TBSV infection. [4] [17]

p22

The p22 protein is a movement protein that is required for the virus to spread from cell to cell. P22 is an RNA-binding protein that is associated with the cell wall and facilitates movement of viral genetic material from one cell to its neighbor through interconnecting plasmodesmata. [4]

Replication

A TBSV virion contains one copy of its positive-sense single-stranded RNA genome, which is linear and lacks a 3' polyadenine tail or 5' cap. Nevertheless, the p33 and p92 proteins are translated directly from genomic RNA. When the genome is replicated, two subgenomic RNA molecules are produced that act as messenger RNA; one from which the p41 (CP) gene is expressed, and one from the p19 and p22 genes are expressed. The overlapping p19 and p22 genes are both translated through the effects of leaky scanning. [4] Several long-distance interactions between linearly well-separated areas of the genome have been identified with functional importance in ensuring efficient replication. [16]

Defective interfering RNA

Defective interfering RNA (DI) molecules are RNAs that are produced from the viral genome but are not competent to infect cells on their own; instead they require coinfection with an intact "helper" virus. TBSV infections often produce significant numbers of DIs from consistent parts of the genome under experimental conditions, but this behavior has not been observed in the wild. Their production is likely to be host specific. Infections that give rise to DIs usually have milder signs. [4] [19]

Related Research Articles

Defective interfering particle

Defective interfering particles (DIPs), also known as defective interfering viruses, are spontaneously generated virus mutants in which a critical portion of the particle's genome has been lost due to defective replication or non-homologous recombination. The mechanism of their formation is presumed to be as a result of template-switching during replication of the viral genome, although non-replicative mechanisms involving direct ligation of genomic RNA fragments have also been proposed. DIPs are derived from and associated with their parent virus, and particles are classed as DIPs if they are rendered non-infectious due to at least one essential gene of the virus being lost or severely damaged as a result of the defection. A DIP can usually still penetrate host cells, but requires another fully functional virus particle to co-infect a cell with it, in order to provide the lost factors.

<i>Reoviridae</i> Family of viruses

Reoviridae is a family of double-stranded RNA viruses. Member viruses have a wide host range, including vertebrates, invertebrates, plants, protists and fungi. They lack lipid envelopes and package their segmented genome within multi-layered capsids. Lack of a lipid envelope has allowed three-dimensional structures of these large complex viruses to be obtained, revealing a structural and likely evolutionary relationship to the cystovirus family of bacteriophage. There are currently 97 species in this family, divided among 15 genera in two subfamilies. Reoviruses can affect the gastrointestinal system and respiratory tract. The name "reo-" is an acronym for "respiratory enteric orphan" viruses. The term "orphan virus" refers to the fact that some of these viruses have been observed not associated with any known disease. Even though viruses in the family Reoviridae have more recently been identified with various diseases, the original name is still used.

Cauliflower mosaic virus (CaMV) is a member of the genus Caulimovirus, one of the six genera in the family Caulimoviridae, which are pararetroviruses that infect plants. Pararetroviruses replicate through reverse transcription just like retroviruses, but the viral particles contain DNA instead of RNA.

Rubella virus Species of virus

Rubella virus (RuV) is the pathogenic agent of the disease rubella, transmitted only between humans via the respiratory route, and is the main cause of congenital rubella syndrome when infection occurs during the first weeks of pregnancy.

A satellite is a subviral agent that depends on the coinfection of a host cell with a helper virus for its replication. Satellites can be divided into two major classes: satellite viruses and satellite nucleic acids. Satellite viruses, which are most commonly associated with plants, are also found in mammals, arthropods, and bacteria. They encode structural proteins to enclose their genetic material, which are therefore distinct from the structural proteins of their helper viruses. Satellite nucleic acids, in contrast, do not encode their own structural proteins, but instead are encapsulated by proteins encoded by their helper viruses. The genomes of satellites range upward from 359 nucleotides in length for satellite tobacco ringspot virus RNA (STobRV).

<i>Geminiviridae</i> Family of viruses

Geminiviridae is a family of plant viruses that encode their genetic information on a circular genome of single-stranded (ss) DNA. There are 520 species in this family, assigned to 14 genera. Diseases associated with this family include: bright yellow mosaic, yellow mosaic, yellow mottle, leaf curling, stunting, streaks, reduced yields. They have single-stranded circular DNA genomes encoding genes that diverge in both directions from a virion strand origin of replication. According to the Baltimore classification they are considered class II viruses. It is the largest known family of single stranded DNA viruses.

<i>Tombusviridae</i> Family of viruses

Tombusviridae is a family of single-stranded positive sense RNA plant viruses. There are three subfamilies, 17 genera, and 95 species in this family. The name is derived from Tomato bushy stunt virus (TBSV).

Tombusvirus is a genus of viruses, in the family Tombusviridae. Plants serve as natural hosts. There are 17 species in this genus. Symptoms associated with this genus include mosaic. The name of the genus comes from Tomato bushy stunt virus.

Agroinfiltration

Agroinfiltration is a method used in plant biology and especially lately in plant biotechnology to induce transient expression of genes in a plant, or isolated leaves from a plant, or even in cultures of plant cells, in order to produce a desired protein. In the method, a suspension of Agrobacterium tumefaciens is introduced into a plant leaf by direct injection or by vacuum infiltration, or brought into association with plant cells immobilised on a porous support, whereafter the bacteria transfer the desired gene into the plant cells via transfer of T-DNA. The main benefit of agroinfiltration when compared to the more traditional plant transformation is speed and convenience, although yields of the recombinant protein are generally also higher and more consistent.

<i>Cowpea chlorotic mottle virus</i> Species of virus

Cowpea chlorotic mottle virus, known by the abbreviation CCMV, is a virus that specifically infects the cowpea plant, or black-eyed pea. The leaves of infected plants develop yellow spots, hence the name "chlorotic". Similar to its "brother" virus, Cowpea mosaic virus (CPMV), CCMV is produced in high yield in plants. In the natural host, viral particles can be produced at 1–2 mg per gram of infected leaf tissue. Belonging to the bromovirus genus, cowpea chlorotic mottle virus (CCMV) is a small spherical plant virus. Other members of this genus include the brome mosaic virus (BMV) and the broad bean mottle virus (BBMV).

<i>Alfalfa mosaic virus</i> Species of virus

Alfalfa mosaic virus (AMV), also known as Lucerne mosaic virus or Potato calico virus, is a worldwide distributed phytopathogen that can lead to necrosis and yellow mosaics on a large variety of plant species, including commercially important crops. It is the only Alfamovirus of the family Bromoviridae. In 1931 Weimer J.L. was the first to report AMV in alfalfa. Transmission of the virus occurs mainly by some aphids, by seeds or by pollen to the seed.

Tombusvirus 3′ UTR region IV

Tombusvirus 3′ UTR is an important cis-regulatory region of the Tombus virus genome.

Tombusvirus 5′ UTR

Tombusvirus 5′ UTR is an important cis-regulatory region of the Tombus virus genome.

Tombusvirus internal replication element (IRE)

In virology, the tombusvirus internal replication element (IRE) is a segment of RNA located within the region coding for p92 polymerase. This element is essential for viral replication; specifically, it is thought to be required at an early stage of replication, such as template recruitment and/or replicase complex assembly.

Rice hoja blanca tenuivirus (RHBV), meaning "white leaf rice virus", is a plant virus in the family Phenuiviridae. RHBV causes Hoja blanca disease (HBD), which affects the leaves of the rice plant Oryza sativa, stunting the growth of the plant or killing it altogether. RHBV is carried by an insect vector, Tagosodes orizicolus, a type of planthopper. The virus is found in South America, Mexico, throughout Central America, the Caribbean region, and the southern United States. In South America, the disease is endemic to Colombia, Venezuela, Ecuador, Peru, Suriname, French Guiana and Guyana.

Potato mop-top virus (PMTV) is a plant pathogenic virus transmitted through the vector Spongospora subterranea that affects potatoes. PMTV belongs to family of Virgaviridae, and the genus Pomovirus. The virus was first identified in 1966 by Calvert and Harrison in Britain, and is now reported in many other potato cultivating regions of the world including U.S.A., Canada, China, Pakistan, Japan, South American countries and many parts of Europe. Many disease management systems have been found to be ineffective against the virus, although a combination of sanitation and vector controls seems to work well.

Turnip crinkle virus (TCV) is a plant pathogenic virus of the family Tombusviridae. It was first isolated from turnip.

Sweet potato feathery mottle virus (SPFMV) is a member of the genus Potyvirus in the family Potyviridae. It is most widely recognized as one of the most regularly occurring causal agents of sweet potato viral disease (SPVD) and is currently observed in every continent except Antarctica. The number of locations where it is found is still increasing; generally, it is assumed that the virus is present wherever its host is. The virus has four strains that are found in varying parts of the world.

Idaeovirus is a genus of positive-sense ssRNA viruses that contains two species: Raspberry bushy dwarf virus (RBDV) and Privet idaeovirus. RBDV has two host-dependent clades: one for raspberries; the other for grapevines. Infections are a significant agricultural burden, resulting in decreased yield and quality of crops. RBDV has a synergistic relation with Raspberry leaf mottle virus, with co-infection greatly amplifying the concentration of virions in infected plants. The virus is transmitted via pollination with RBDV-infected pollen grains that first infect the stigma before causing systemic infection.

RNA silencing suppressor p19 Viral protein

RNA silencing suppressor p19 is a protein expressed from the ORF4 gene in the genome of tombusviruses. These viruses are positive-sense single-stranded RNA viruses that infect plant cells, in which RNA silencing forms a widespread and robust antiviral defense system. The p19 protein serves as a counter-defense strategy, specifically binding the 19- to 21-nucleotide double-stranded RNAs that function as small interfering RNA (siRNA) in the RNA silencing system. By sequestering siRNA, p19 suppresses RNA silencing and promotes viral proliferation. The p19 protein is considered a significant virulence factor and a component of an evolutionary arms race between plants and their pathogens.

References

  1. ↑ Hopper, P; Harrison, SC; Sauer, RT (25 August 1984). "Structure of tomato bushy stunt virus. V. Coat protein sequence determination and its structural implications". Journal of Molecular Biology. 177 (4): 701–13. doi:10.1016/0022-2836(84)90045-7. PMID   6481803.
  2. ↑ Mahy, Brian W. J.; Regenmortel, Marc H. V. Van (15 October 2009). Desk Encyclopedia of Plant and Fungal Virology. Academic Press. pp. 445–. ISBN   978-0-12-375148-5 . Retrieved 4 December 2012.
  3. 1 2 3 Scholthof, Herman B. (6 March 2006). "The Tombusvirus-encoded P19: from irrelevance to elegance". Nature Reviews Microbiology. 4 (5): 405–411. doi:10.1038/nrmicro1395. PMID   16518419. S2CID   30361458.
  4. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 Yamamura, Y; Scholthof, HB (1 September 2005). "Tomato bushy stunt virus: a resilient model system to study virus-plant interactions". Molecular Plant Pathology. 6 (5): 491–502. doi:10.1111/j.1364-3703.2005.00301.x. PMID   20565674.
  5. 1 2 3 4 5 Martelli, G.P.; Russo, M.; Rubino, L. (December 2001). "Tomato bushy stunt virus". Descriptions of Plant Viruses. Association of Applied Biologists. Archived from the original on 11 August 2020. Retrieved 15 December 2016.
  6. ↑ Panavas, Tadas; Nagy, Peter D (15 September 2003). "Yeast as a model host to study replication and recombination of defective interfering RNA of Tomato bushy stunt virus". Virology. 314 (1): 315–325. doi: 10.1016/S0042-6822(03)00436-7 . PMID   14517084.
  7. ↑ Balique, Fanny; Lecoq, Hervé; Raoult, Didier; Colson, Philippe (20 April 2015). "Can Plant Viruses Cross the Kingdom Border and Be Pathogenic to Humans?". Viruses. 7 (4): 2074–2098. doi: 10.3390/v7042074 . PMC   4411691 . PMID   25903834.
  8. ↑ "Integrated Pest Management Program". UC Pest Management Guidelines. University of California Division of Agriculture and Natural Resources. December 2013. Retrieved 16 December 2016.
  9. ↑ "ICTV Taxonomy History for Tomato bushy stunt virus". International Committee on Taxonomy of Viruses. July 2015. Retrieved 16 December 2016.
  10. ↑ Harrison, B. D.; Finch, J. T.; Gibbs, A. J.; Hollings, M.; Shepherd, R. J.; Valenta, V.; Wetter, C. (1 August 1971). "Sixteen groups of plant viruses". Virology. 45 (2): 356–363. doi:10.1016/0042-6822(71)90336-9. PMID   5106891.
  11. ↑ Rossmann, Michael G. (1 May 2013). "Structure of viruses: a short history". Quarterly Reviews of Biophysics. 46 (2): 133–180. doi:10.1017/S0033583513000012. ISSN   0033-5835. PMID   23889891. S2CID   33838033.
  12. ↑ Harrison, S. C.; Olson, A. J.; Schutt, C. E.; Winkler, F. K.; Bricogne, G. (23 November 1978). "Tomato bushy stunt virus at 2.9 Å resolution". Nature. 276 (5686): 368–373. Bibcode:1978Natur.276..368H. doi:10.1038/276368a0. PMID   19711552. S2CID   4341051.
  13. ↑ Hellemans, Alexander; Bunch, Bryan H. (1988). The timetables of science: a chronology of the most important people and events in the history of science . Simon and Schuster. p. 582. ISBN   978-0-671-62130-8 . Retrieved 7 September 2020.
  14. ↑ Hearne, Patrick Q.; Knorr, David A.; Hillman, Bradley I.; Morris, Thomas J. (1 July 1990). "The complete genome structure and synthesis of infectious RNA from clones of tomato bushy stunt virus". Virology. 177 (1): 141–151. doi:10.1016/0042-6822(90)90468-7. PMID   2353450.
  15. ↑ Wagner, Edward K.; Hewlett, Martinez J.; Bloom, David C.; David Camerini (6 November 2007). Basic Virology. John Wiley & Sons. pp. 268–. ISBN   9781405147156 . Retrieved 4 December 2012.
  16. 1 2 Wu, Baodong; Grigull, Jörg; Ore, Moriam O.; Morin, Sylvie; White, K. Andrew (23 May 2013). "Global Organization of a Positive-strand RNA Virus Genome". PLOS Pathogens. 9 (5): e1003363. doi:10.1371/journal.ppat.1003363. ISSN   1553-7374. PMC   3662671 . PMID   23717202.
  17. 1 2 Scholthof, Herman B.; Scholthof, Karen-Beth G.; Kikkert, Marjolein; Jackson, A.O. (1995). "Tomato Bushy Stunt Virus Spread Is Regulated by Two Nested Genes That Function in Cell-to-Cell Movement and Host-Dependent Systemic Invasion". Virology. 213 (2): 425–38. doi: 10.1006/viro.1995.0015 . PMID   7491767.
  18. ↑ Jones, Richard W.; Jackson, A.O.; Morris, Thomas J. (1990). "Defective-interfering RNAs and elevated temperatures inhibit replication of tomato bushy stunt virus in inoculated protoplasts". Virology. 176 (2): 539–45. doi:10.1016/0042-6822(90)90024-L. PMID   2345965.
  19. ↑ Scholthof, Karen-Beth G.; Scholthof, Herman B.; Jackson, Andrew O. (1 August 1995). "The Effect of Defective Interfering RNAs on the Accumulation of Tomato Bushy Stunt Virus Proteins and Implications for Disease Attenuation". Virology. 211 (1): 324–328. doi: 10.1006/viro.1995.1410 . PMID   7645230.
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