Cadang-cadang

Last updated
Coconut cadang-cadang viroid
Virus classification OOjs UI icon edit-ltr.svg
(unranked): Viroid
Family: Pospiviroidae
Genus: Cocadviroid
Species:
Coconut cadang-cadang viroid

Cadang-cadang is a disease caused by Coconut cadang-cadang viroid (CCCVd), a lethal viroid of several palms including coconut (Cocos nucifera), African oil palm ( Elaeis guineensis ), anahaw ( Saribus rotundifolius ), and buri ( Corypha utan ). The name cadang-cadang comes from the word gadang-gadang that means dying in Bicol. [1] It was originally reported on San Miguel Island in the Philippines in 1927/1928. "By 1962, all but 100 of 250,000 palms on this island had died from the disease," indicating an epidemic. [2] Every year one million coconut palms are killed by CCCVd and over 30 million coconut palms have been killed since Cadang-cadang was discovered. CCCVd directly affects the production of copra, a raw material for coconut oil and animal feed. Total losses of about 30 million palms and annual yield losses of about 22,000 metric tons (22,000 long tons; 24,000 short tons) of copra have been attributed to Cadang-cadang disease in the Philippines. [3]

Contents

Characteristics

Viroids are small, single-stranded RNA molecules, ranging from 246 to 375 nucleotides long. Unlike viruses, they do not code for protein coats but contain genes for autonomous replication. With abilities to cause serious disease, they are more commonly found in a latent stage, and their mode of infection is mainly mechanical, though documented cases exist of vertical transmission through pollen and seed. [4] The sequence and structure prediction of CCCVd has been documented. There are four low-molecular-weight RNA species (ccRNAs) found associated with cadang-cadang disease. [5] Of the four, two are related with the early stage of the disease: ccRNA 1 fast and ccRNA 2 fast. After several years, two other species appear and predominate: ccRNA 1 slow and ccRNA 2 slow. Moreover, they share sequence homology with other viroids. [2]

Conditions for a viroid to infect its host include wounds on the host or infected pollen grain deposited into an ovule. [6] Not all of the mentioned conditions pertain to cadang-cadang.

Tinangaja disease is caused by coconut trinangaja viroid (CTiVd), which has 64% sequence homology with CCCVd. This disease has been found in Guam. Coconuts from Asia and the South Pacific have been found to have viroids with similar (homologous) nucleic acid sequences of CCCVd. The pathogenicity of CTiVd is uncertain. [7] Coconut cadang-cadang viroid, also known as CCCVd, is responsible for a lethal disease of coconut plant first reported in the early 1930 in the Philippines. CCCVd is the smallest known pathogen and it is biologically distinct from other viroids; it consists of circular or lineal single-stranded RNA with a basic size of 246 or 247, it is thought it can be transmitted by seed or pollen (with low transmission rates) and occur in almost all plant parts. Once infected, coconut palm shows yellow leaf spots and nut production ceases; from appearance of first symptoms to tree death, time ranges from around 8 to 16 years, but the pest is generally greater in older plants. It is estimated that over 30 million coconut palms have been killed by cadang-cadang since it was first recognised and the loss of production is valued at about $80 – $100 for each planting site occupied by an infected tree.[ citation needed ]

Scheme of the central domain of the viroid CCCVd.pdf
Scheme of the central domain of the viroid
Scheme of a pospiviroid Estructura de un pospiviroid.pdf
Scheme of a pospiviroid

Molecular structure

CCCVd are small, circular, and single-stranded. They cannot replicate themselves, and therefore are completely dependent on a host.[ citation needed ]

CCCVd have a sequence of 246 nucleotides, 44 of which are common with most viroids. [2] CCCVd can add a cytosine residue in the 197 position and increase the size to 247 nucleotides. It is known that forms of CCCVd with 247 nucleotides cause severe symptoms. Their minimum size is 246, but they can produce forms from 287 to 301 nucleotides. [1]

In CCCVd, changes in molecular forms are related to the steps of the disease. There are four different RNAs found in CCCVd, two of them fast and the other two slow (the difference between fast and slow RNA is their mobilities in electrophoresis gel). In the early stages of the disease, RNA fast 1 and RNA fast 2 appear, while in the late stages RNA slow 1 and RNA slow 2 are detected.[ citation needed ]

Geographical distribution

The CCCVd is widely spread in Philippines and it is mostly found in Bicol Region, Masbate, Catanduanes, Samar and other smaller islands in the zone. It is known that the present northernmost boundary is at the latitude of Manila and the southernmost at the latitude of Homonhon Island. This fact is important due to the proximity of the disease to the major coconut and oil palm growing area of Mindanao. [8] An isolated focus of infection has been found on the Solomon Islands, in Oceania.[ citation needed ]

The available data at the present suggests that the epidemiology of cadang-cadang viroid may not be spreading into any specific route.[ citation needed ]

Variants

In Guam, a similar viroid known as coconut tinangaja viroid (CTiVd) has been found that causes a similar disease named tinangaja disease. This viroid has 64% sequence homology with the cadang-cadang viroid. [9] There are other related viroids with the CCCVd, which are found in Asia and the South Pacific. They have a high degree of homology but the pathogenicity is uncertain. [10]

Transmission

The mode of natural inoculation of the viroid is unknown. There has been evidence that the transmission through pollen and seed can occur but they have a very low transmission rates: progenies of healthy palms pollinated with diseased pollen, exhibited disease symptoms 6 years after germination. [11]

CCCVd can spread through mechanical inoculation primarily through contaminated farm tools such as harvesting scythes or machetes, due to the improper sanitary conditions. [12] The efficiency of the mechanical inoculation has been influenced by factors such as the age of the test plant and the mode of inoculation.[ citation needed ]

Experimental transmission of the CCCVd using insects as vector has been unsuccessful although there are few evidences that the transmission of the viroid might be related to the wounds of coelopteran insects, but this has not been properly investigated. [12]

The natural hosts of cadang-cadang identified are Cocos nucifera , Corypha utan , Elaeis guineensis and Roystonea regia . The experimental hosts are Adonidia merrillii , Areca catechu , Caryota cumingii , Dypsis lutescens , Saribus rotundifolius , Phoenix dactylifera , Ptychosperma macarthurii and Roystonea regia . [13]

Process of detection of CCCVd Palmeras.pdf
Process of detection of CCCVd

Detection

The diagnosis by symptoms is not reliable enough so it's better to do a molecular diagnosis based in test samples. Some of these methods (like Dot-blot hybridisation) allow the scientists to detect the viroid even six months before noticing the first symptoms.

The first step is the purification to obtain the nucleic acids of the plant cells. The leaves of the plant located four or more below the spare leaf are cut. Afterwards, they are blended (homogenize) with sodium sulfite. Then the extract is filtered and clarified by centrifugation (10.000 g during 10 minutes). The next step is to add polyethylene glycol (PEG). Finally, after nearly two hours of incubation at 4 °C, and after another centrifugation (at low speed) the nucleic acids can be extracted by chloroform procedures, for example.

When approximately 1 g of coconut tissue has been purified, the electrophoresis method can be started, which will help to identify the viroid by its relative mobility. [7] The CCCVd is analysed in one or two dimensional polyacrylamide gels with a silver stain.

The viroid can also be detected by a more sensitive method called dot blot molecular hybridization. [14] In this method CCCVd is amplified by the PCR (polymerase chain reaction) and the clones of CCCVd are used as templates to synthesize a complementary DNA or RNA chain. These sequences are radioactively labelled so when they are put over the samples with the intention to analyse (on a supporting membrane) and exposed to x-ray film, then if CCCVd is present it will appear as a dark colour. This dark tonality only appears when nucleic acid hybridisation occurs.[ citation needed ]

Pharmacology and treatment

Coconut cadang-cadang disease has no treatment yet. However, chemotherapy with antibiotics has been tried with tetracycline solutions; antibiotics failed trying to alter progress of the disease since they had no significant effect on any of the studied parameters. When the treated plants were at the early stage, tetracycline injections failed to prevent the progression of the palms to more advanced stages, nor did they affect significantly the mean number of spathes or nuts. Penicillin treatment had no apparent improvement either.[ citation needed ]

Control strategies are elimination of reservoir species, vector control, mild strain protection and breeding for host resistance. [15] Eradication of diseased plants is usually performed to minimize spread but is of dubious efficacy due to the difficulties of early diagnosis as the virus etiology remains unknown and the one discovered are the three main stages in the disease development.[ citation needed ]

Easily confused pests

Coconut Cadang Cadang Viroid (CCCVd) can be confused with another viroid called Coconut Tinangaja Viroid (CTiVd). That is because both viroids have 64% of their sequence of nucleotides in common. They both affect coconut palm, and infected plants have similar symptoms: spots on the leaves reduced top, yellow palms and even death. [16]

There are few differences between both viroids in the effects caused on fruit: CTiVd causes small nuts, while CCCVd causes round and reduced nuts. Moreover, CTiVd has 254 nucleotides of length, while CCCVd has 246.

Symptoms

Symptoms of cadang-cadang develop slowly over 8 to 15 years making it difficult to diagnose at an early time. [6] There are three main “stages” of defined series of characteristics: early, medium, and late stages. [17] The first symptoms in the early stage develop within two to four years of infection. [17] These symptoms include scarification of the coconuts which also become rounded. The leaves (fronds) display bright yellow spots. About two years later, during the medium stage, [18] the inflorescences become stunted and eventually killed, so no more coconuts are produced. Yellow spots are larger and in greater abundance to give the appearance of chlorosis. During the final stage, roughly 6 years after the first symptoms are recorded, the yellow/bronze fronds start to decrease in size and number. Finally, all the leaves coalesce, leaving just the trunk of the palm “standing like a telephone pole”. [6]

Palms under 10 years of age are rarely affected by cadang-cadang; the incidence of disease increases until about 40 years of age and then plateaus. [19] "No recovery has ever been observed, and the disease is always fatal". [4] African oil palm has similar symptoms as coconut but also have orange spotting on palms. [20]

Environment

Geographical location

Philippines: Southern Luzon, Samar, Masbate, and other small islands. Tinangaja was found in Guam on Mariana Islands. [19] Evidence shows that CCCVd is negatively correlated with altitude. [3]

Dispersal

The CCCVd viroid can be transmitted by pollen, seed, and mechanical transmission; it infects almost all parts of the host after flowering.[ citation needed ]

Insect vectors

No insect vector is known at this time, and rate of dispersal is not related to proximity of clusters.

Control

No definite control measures exist at the present.[ citation needed ]

Related Research Articles

Viroids are small single-stranded, circular RNAs that are infectious pathogens. Unlike viruses, they have no protein coating. All known viroids are inhabitants of angiosperms, and most cause diseases, whose respective economic importance to humans varies widely. A recent metatranscriptomics study suggests that the host diversity of viroids and other viroid-like elements is broader than previously thought and that it would not be limited to plants, encompassing even the prokaryotes.

Virusoids are circular single-stranded RNA(s) dependent on viruses for replication and encapsidation. The genome of virusoids consists of several hundred (200–400) nucleotides and does not code for any proteins.

<span class="mw-page-title-main">Theodor Otto Diener</span> American plant pathologist (1921–2023)

Theodor Otto Diener was a Swiss-American plant pathologist. In 1971, he discovered that the causative agent of the potato spindle tuber disease is not a virus, but a novel agent, which consists solely of a short strand of single-stranded RNA without a protein capsid, eighty times smaller than the smallest viruses. He proposed to name it, and similar agents yet to be discovered, viroids. Viroids displaced viruses as the smallest known infectious agents.

The potato spindle tuber viroid (PSTVd) was the first viroid to be identified. PSTVd is a small, single stranded circular RNA molecule closely related to the chrysanthemum stunt viroid. Present within the viroidal RNA is the Pospiviroid RY motif stem loop common to its genus. The natural hosts are potatoes and tomatoes. All potatoes and tomatoes are susceptible to PSTVd and there is no form of natural resistance. Natural infections have also been seen in avocados and infections in other solanaceous crops have been induced in the laboratory. Until 2017 PSTVd was thought to be unable to infect Solanum sisymbriifolium. Then in May seeds exported by a Dutch company were noticed to be infected. These seeds were shipped from the company, but had been originally bred to their specifications in two Asian countries. Pstv also causes Tomato bunchy top and is seed transmitted in tomato.

The Pospiviroidae are a incertae sedis family of ssRNA viroids with 5 genera and 39 species, including the first viroid to be discovered, PSTVd, which is part of genus Pospiviroid. Their secondary structure is key to their biological activity. The classification of this family is based on differences in the conserved central region sequence. Pospiviroidae replication occurs in an asymmetric fashion via host cell RNA polymerase, RNase, and RNA ligase. Its hosts are plants, specifically dicotyledons and some monocotyledons.

Peach latent mosaic viroid is a species of the genus Pelamoviroid, which belongs to the family Avsunviroidae. This family is characterized as having chloroplastic viroids with hammerhead ribozymes. Peach latent mosaic viroid is a 336-351nt circular RNA which has a branched formation. This branched formation is stabilised by a pseudoknot between two kissing loops. Peach latent mosaic viroid was first described in the 1980s in Spain by a group of scientists.

<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.

<i>Avsunviroidae</i> Family of viruses

The Avsunviroidae are a family of viroids. There are four species in three genera. They consist of RNA genomes between 246 and 375 nucleotides in length. They are single-stranded covalent circles and have intramolecular base pairing. All members lack a central conserved region.

Ceratocystis paradoxa or Black Rot of Pineapple is a plant pathogen that is a fungus, part of the phylum Ascomycota. It is characterized as the teleomorph or sexual reproduction stage of infection. This stage contains ascocarps, or sacs/fruiting bodies, which contain the sexually produced inoculating ascospores. These are the structures which are used primarily to survive long periods of time or overwinter to prepare for the next growing season of its host. Unfortunately, the sexual stage is not often seen in the natural field but instead the anamorph, or asexual stage is more commonly seen. This asexual stage name is Thielaviopsis paradoxa and is the common cause of Black rot or stem-end rot of its hosts.

Hop latent viroid is a viroid, which is known to cause the Dudding Disease in hemp and cannabis. It is a non-capsulated strand of RNA and an obligate parasite that requires the presence of a compatible host for its survivability. It can have minor effects on hop quality, but has shown to cause severe stunting in hemp and cannabis. Due to its ability to remain undetected, it has become an issue of significant risk for some hemp and cannabis cultivars. Studies regarding this viroid and its ability to infiltrate its plant host are well underway; however, addressing measures to reduce its introduction into growing environments is still challenging.

Potato virus Y (PVY) is a plant pathogenic virus of the family Potyviridae, and one of the most important plant viruses affecting potato production.

Prune dwarf virus (PDV) is an economically important plant pathogenic virus affecting Prunus species globally. PDV is found worldwide due to easy transmission through seed, pollen, and vegetative propagation. The virus is in the family Bromoviridae an important family of plant RNA viruses containing six genera, including Alfamovirus, Ilarvirus, Bromovirus, Amularvirus, Oleavirus, and Cucumovirus. PDV belongs to the genera Ilarvirus. It can cause dwarfism of leaves on certain prune and plum plants. It will also cause yellows in sour cherry, especially when present with Prunus necrotic ringspot virus. There are no known transmission vectors, though the pollen of infected cherry trees has been found to infect other cherry trees a small percent of the time.

<i>Tobacco ringspot virus</i> Species of virus

Tobacco ringspot virus (TRSV) is a plant pathogenic virus in the plant virus family Secoviridae. It is the type species of the genus Nepovirus. Nepoviruses are transmitted between plants by nematodes, thrips, mites, grasshoppers, and flea beetles. TRSV is also easily transmitted by sap inoculation and transmission in seeds has been reported. In recent cases it has also been shown to appear in bees, but no transmission to plants from bees has been noted.

<i>Strawberry vein banding virus</i> Species of virus

Strawberry vein banding virus (SVBV) is a plant pathogenic virus and a member of the family Caulimoviridae.

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.

<span class="mw-page-title-main">Karl Maramorosch</span>

Karl Maramorosch was an Austrian-born American virologist, entomologist, and plant pathologist. A centenarian and polyglot, he conducted research on viruses, mycoplasmas, rickettsiae, and other micro-organisms; and their transmission to plants through insect vectors in many parts of the world. He is the co-author of a textbook on techniques in virology and is the author of numerous papers on the biology and ecology of plant viruses, their hosts, and vectors. He received the Wolf Prize in Agriculture in 1980 for his contribution to the study of crop pathogens.

Grapevine virus A (GVA) is a moderately common genetic virus that affects Vitis vinifera and American Vitis grapevine species throughout the world and can be fatal if not treated. Grapevine virus A is in the family Betaflexiviridae and genus Vitivirus. The common name for this virus is grapevine closterovirus. Common symptoms in infected grapevines include stem pitting. Although there is a treatment available to cure infected grapevines, it is not one hundred percent effective, so preventative measures are the best solution to the virus. Every inhabited continent on the globe has had breakouts of grapevine closterovirus due to the complex genetic makeup of the virus. Grapevine virus A has a single-stranded RNA genome, which is similar to that of Grapevine virus B. There are multiple strains of the virus that vary both molecularly and biologically which account for the slightly different symptoms exhibited by infected plants.

Cassava brown streak virus is a species of positive-strand RNA viruses in the genus Ipomovirus and family Potyviridae which infects plants. Member viruses are unique in their induction of pinwheel, or scroll-shaped inclusion bodies in the cytoplasm of infected cells. Cylindrical inclusion bodies include aggregations of virus-encoded helicase proteins. These inclusion bodies are thought to be sites of viral replication and assembly, making then an important factor in the viral lifecycle. Viruses from both the species Cassava brown streak virus and Ugandan cassava brown streak virus (UCBSV), lead to the development of Cassava Brown Streak Disease (CBSD) within cassava plants.

<span class="mw-page-title-main">Tomato spotted wilt orthotospovirus</span> Species of virus

Tomato spotted wilt orthotospovirus (TSWV) is a spherical negative-sense RNA virus. Transmitted by thrips, it causes serious losses in economically important crops and it is one of the most economically devastating plant viruses in the world.

<span class="mw-page-title-main">Oryctes rhinoceros nudivirus</span> Virus and biocontrol agent of Oryctes rhinoceros

The Oryctes rhinoceros nudivirus (OrNV) is a member of the species Alphanudivirus oryrhinocerotis in the family Nudiviridae. It causes lethal infections in larvae and adults of the coconut rhinoceros beetle, a serious pest of coconut and oil palms in tropical Asia and the Pacific. The virus was discovered by Alois Huger in 1963 while searching for diseases of O. rhinoceros in Malaysia. It has been demonstrated to be an effective biological control agent against this beetle pest.

References

  1. 1 2 Hanold, D.; Randles, J. W. (1991). "Coconut Cadang-Cadang Disease and Its Viroid Agent". Plant Disease . 75 (4). American Phytopathological Society: 330–335. doi:10.1094/PD-75-0330. (Waite Agricultural Research Institute, University of Adelaide Glen Osmond, South Australia)
  2. 1 2 3 Haseloff J.; Mohamed N.A.; Symons R.H. (1982). "Viroid RNAs of cadang-cadang disease of coconuts". Nature . 299 (5881): 316–321. Bibcode:1982Natur.299..316H. doi:10.1038/299316a0. S2CID   4232530.
  3. 1 2 Zelazny B (1980). "Ecology of Cadang-Cadang Disease of Coconut Palm in the Philippines". Phytopathology . 70 (8): 700–703. doi:10.1094/phyto-70-700.
  4. 1 2 Maramorosch, K. (1991). Viroids and Satellites: Molecular Parasites at the Frontier of Life. Boston: CRC Press. ISBN   0-8493-6783-2.
  5. ↑ Imperial J.S.; Rodrieguez J.B.; Randles J.W. (1981). "Variation in the Viroid-Like RNA Associated With Cadang-Cadang Disease: Evidence for an Increase in Molecular Weight With Disease Progress". Journal of General Virology . 56: 77–85. doi: 10.1099/0022-1317-56-1-77 .
  6. 1 2 3 Agrios 2005, pages 822-823.
  7. 1 2 Hanold, D.; Randles, J. W. (1991). "Detection of coconut cadang-cadang viroid-like sequences in oil and coconut palm and other monocotyledons in the south-west Pacific". Annals of Applied Biology . 118 (1). Association of Applied Biologists/Wiley-Blackwell: 139–151. doi:10.1111/j.1744-7348.1991.tb06092.x. ISSN   0003-4746.
  8. ↑ Randles, J.W., Hanold, D., Pacumba, E.P., and Rodriguez, M. J. B. Cadang-cadang disease of coconut palm. In: Plant Diseases of International Importance. A. N. Mukhopadhyay, J. Kumar, H.S. Chabue, and U. S. Singh, eds. Pretice Hall, Englewood Cliffs, NJ. In press. 1991
  9. ↑ Boccardo, G., Beaver, R. G., Randles, J.W., and Imperial, J.S. Tinangaja and bristle top, coconut diseases of uncertain etiology in Guam and their relationship to cadang-cadang disease of coconut in Philippines.1981
  10. ↑ EPPO Quarantine Pest and CABI. Coconut cadang-cadang viroid. Data sheets on Quarantine Pests 1978
  11. ↑ Pacumbaba, E.B.; Zelazny, B.; Orense, J.C. (Philippine Coconut Authority, Banao, Guinobatan, Albay (Philippines). Albay Research Center. Pollen and seed transmission of the coconut cadang-cadang viroid. May 1992.
  12. 1 2 Zelazny, B., Randles, J. W., Boccardo, G., and Imperial J.S 1982. The viroid nature of the cadang-cadang disease of coconut palm. Scientia Flipinas, 1979
  13. ↑ Batugal, P., Ramanatha Rao, V., Oliver, J. (eds.) Coconut Genetic Resources. 2005
  14. ↑ Symons R.H. (1985). "Dot blot procedure with 32P DNA probes for the sensitive detection of avocado sunblotch and other viroids in plants". Journal of Virological Methods. 10 (2): 87–98. doi:10.1016/0166-0934(85)90094-1. PMID   3980666.
  15. ↑ Boccardo G., Randles J. W., Retuerma M. L. and Rillo Erlinda P., Transmission of the RNA Species Associated with Cadang-Cadang of coconut plant and the Insensivity of the Disease to Antibiotics, 1977.
  16. ↑ Bigornia, Q12 Philippine Journal of Coconout Studies, 1977.
  17. 1 2 Philippine Coconut Authority. Coconut Cadang-Cadang Disease Primer. Philippine Coconut Authority. PCA. Web. 23 Oct. 2011. <http://www.pca.da.gov.ph Archived 2011-10-09 at the Wayback Machine >.
  18. ↑ European and Mediterranean Plant Protection Organization, CABI. (2008). Coconut Cadang-cadang viroid [Data file]. Retrieved from http://www.eppo.org/QUARANTINE/virus/Coconut_cadang_cadang_viroid/CCCVD0_ds.pdf Archived 2010-07-13 at the Wayback Machine
  19. 1 2 Randles, J.W.; Imperial, J.S. (July 1984). Coconut cadang-cadang viroid. Retrieved from http://www.dpvweb.net/dpv/showadpv.php?dpvno=287 Archived 2015-09-23 at the Wayback Machine
  20. ↑ Coconut cadang-cadang viroid. (2008). [Caption under Cadang-cadang photo May 4, 2010]. Coconut Cadang-cadang viroid: cocadviroid CCCVd. Retrieved from http://www.invasive.org/browse/detail.cfm?imgnum=0656010 on 20 Now. 2011.
  21. ↑ Stefan Riedel, MD (January 2005). "Edward Jenner and the history of smallpox and vaccination". Proc (Bayl Univ Med Cent). 18 (1): 21–25. doi:10.1080/08998280.2005.11928028. PMC   1200696 . PMID   16200144.
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.