The genus Begomovirus contains more than 200 species and belongs to the taxonomic family Geminiviridae. They are plant viruses that as a group have a very wide host range, infecting dicotyledonous plants. Worldwide they are responsible for a considerable amount of economic damage to many important crops such as tomatoes, beans, squash, cassava and cotton.
Virus particles are non-enveloped. The nucleocaspid is 38 nanometers (nm) long and 15–22 nm in diameter. While particles have basic icosaherdal symmetry, they consist of two incomplete icosahedra—missing one vertex—joined together. There are 22 capsomeres per nucleocapsid.
Single stranded closed circular DNA. Many begomoviruses have a bipartite genome: this means that the genome is segmented into two segments (referred to as DNA A and DNA B) that are packaged into separate particles. Both segments are generally required for successful symptomatic infection in a host cell but DNA B is dependent for its replication upon DNA A, which can in some begomoviruses apparently cause normal infections on its own.
The DNA A segment typically encodes five to six proteins including replication protein Rep, coat protein and transport and/or regulatory proteins. This component is homologous to the genomes of all other geminiviruses. The proteins endcoded on it are required for replication (Rep), control of gene expression, overcoming host defenses, encapsidation (coat protein) and insect transmission. The DNA B segment encodes two different movement proteins. These proteins have functions in intra- and intercellular movement in host plants.
The A and B components share little sequence identity with the exception of a ~200 nucleotide sequence with typically >85% identity known as the common region. This region includes an absolutely conserved (among geminiviruses) hairpin structure and repeated sequences (known as 'iterons') that are the recognition sequences for binding of the replication protein (Rep). Within this loop there is a nonanucleotide sequence (TAATATTAC) that acts as the origin (ori) of virion strand DNA replication.
Component exchange (pseudorecombination) occurs in this genus. The usual mechanism of pseudorecombination is by a process known as 'regulon grafting': the A component donates its common region by recombination to the B component being captured. This results in a new dependent interaction between two components.
The proteins in this genus may lie either on the sense strand (positive orientation) or its complement (negative orientation).
- Segment A
- V1 (R1)—positive orientation: Coat protein—29.7 kiloDaltons (kDa)
- V2—positive orientation: Movement protein (precoat ORF)—12.8 kDa
- C1 (L1)—negative orientation: Replication initiation protein (Rep)—40.2 kDa
- C2: (L2)—negative orientation: Transcription activator protein (TrAP)—19.6 kDa
- C3: (L3)—negative orientation: Replication enhancer—15.6 kDa
- C4:—negative orientation: May determine symptom expression—12.0 kDa
- Segment B
- V1 (R1)—positive orientation: Nuclear shuttle protein—33.1 kDa
- C1 (L1)—negative orientation: Movement protein—29.6 kDa
Smaller than unit length virus components—deletion mutants—are common in infections. These are known as defective interfering (di) DNAs due to their capacity to interfere with virus infection. They reduce virus DNA levels and symptom severity.
The two components of the genome have very distinct molecular evolutionary histories and likely to be under very different evolutionary pressures. The DNA B genome originated as a satellite that was captured by the monopartite progenitor of all extant bipartite begomoviruses and has subsequently evolved to become an essential genome component.
More than 133 begomovirus species having monopartite genomes are known: all originate from the Old World. No monopartite begomoviruses native to the New World have yet been identified.
Phylogenetic analysis is based on the A component. B components may be exchanged between species and may result in new species.
Analysis of the genus reveals a number of clades. The main division is between the Old and New World strains. The Old World strains can be divided into African, Indian, Japanese and other Asian clades with a small number of strains grouping outside these. The New World strains divide into Central and Southern America strains.
Along with these main groupings are a number of smaller clades. One group infecting a range of legumes originating from India and Southeast Asia (informally 'Legumovirus') and a set of viruses isolated from Ipomoea species originating from America, Asia and Europe (informally 'Sweepovirus') appear to be basal to all the other species. Two species isolated from Corchorus from Vietnam (informally 'Corchovirus') somewhat unexpectedly group with the New World species.
The virus is obligately transmitted by an insect vector, which can be the whitefly Bemisia tabaci or can be other whiteflies. This vector allows rapid and efficient propagation of the virus because it is an indiscriminate feeder.
The type species Potato yellow mosaic virus (PYMV) is a Begomovirus, first identified in the late 1980s, that causes an infection in tomatoes. Disease is manifested in the infected plant as yellow mosaic or mottling, leaf distortion and crinkling and stunting. In Trinidad this disease in tomato is endemic and causes an estimated yield loss of 50–60%. PYMV disease is also an economical problem in the Caribbean. The type species Bean golden yellow mosaic virus (BGYMV) also belongs to the Begomovirus genus. It causes a serious disease in bean species within Central America, the Caribbean and southern Florida.
- Zaim M, Kumar Y, Hallan V, Zaidi AA (2011) Velvet bean severe mosaic virus: a distinct begomovirus species causing severe mosaic in Mucuna pruriens (L.) DC. Virus Genes 43(1):138–146
- Zambrano K, Geraud-Pouey F, Chirinos D, Romay G, Marys E (2011) Tomato chlorotic leaf distortion virus, a new bipartite begomovirus infecting Solanum lycopersicum and Capsicum chinense in Venezuela. Arch Virol
- Fauquet, C. M., Briddon, R. W., Brown, J. K., Moriones, E., Stanley, J., Zerbini, M., and Zhou, X. (2008). "Geminivirus strain demarcation and nomenclature". Archives of Virology 153 (4): 783–821. doi:10.1007/s00705-008-0037-6. PMID 18256781.
- Pita JS, Fondong VN, Sangaré A, Otim-Nape GW, Ogwal S, Fauquet CM (2001). "Recombination, pseudorecombination and synergism of geminiviruses are determinant keys to the epidemic of severe cassava mosaic disease in Uganda". J Gen Virol 82 (3): 655–65.
- Briddon RW, Patil BL, Bagewadi B, Nawaz-ul-Rehman MS, Fauquet CM (2010) Distinct evolutionary histories of the DNA-A and DNA-B components of bipartite begomoviruses. BMC Evol Biol 10:97
- Funayama, Sachiko; Terashima, I; Yahara, T (2001). "Effects of Virus Infection and Light Environment on Population Dynamics of Eupatorium makinoi (Asteraceae)". American Journal of Botany 88 (4): 616–622. doi:10.2307/2657060. JSTOR 2657060. PMID 11302846.
Mansoor S, Briddon RW, Zafar Y, Stanley J (March 2003). "Geminivirus disease complexes: an emerging threat". Trends Plant Sci. 8 (3): 128–34. doi:10.1016/S1360-1385(03)00007-4. PMID 12663223.
Briddon RW, Stanley J (January 2006). "Subviral agents associated with plant single-stranded DNA viruses". Virology 344 (1): 198–210. doi:10.1016/j.virol.2005.09.042. PMID 16364750.
Sinisterra XH, McKenzie CL, Hunter WB, Powell CA, Shatters RG (May 2005). "Differential transcriptional activity of plant-pathogenic begomoviruses in their whitefly vector (Bemisia tabaci, Gennadius: Hemiptera Aleyrodidae)". J. Gen. Virol. 86 (Pt 5): 1525–32. doi:10.1099/vir.0.80665-0. PMID 15831966.
Hunter WB, Hiebert E, Webb SE, Tsai JH, Polston JE (1998). "Location of geminiviruses in the whitefly Bemisia tabaci (Homoptera: Aleyrodidae". Plant Disease 82 (10): 1147–51. doi:10.1094/PDIS.19220.127.116.117.
Cassava mosaic virus
African cassava mosaic virus (ACMV), East African cassava mosaic virus (EACMV), and South African cassava mosaic virus (SACMV) are distinct species of circular single-stranded DNA viruses that are whitefly-transmitted and primarily infect cassava plants. These have thus far only been reported from Africa; related species of viruses (Indian cassava mosaic virus, ICMV) are found in India and neighbouring islands (Sri Lankan cassava mosaic virus, SLCMV), though cassava is cultivated in Latin America as well as South East Asia. Nine species of cassava-infecting geminiviruses have been identified between Africa and India based on genomic sequencing and phylogenetic analysis. This number will probably grow due to a high rate of natural transformation associated with CMV.
The viruses are members of the Family Geminiviridae and the Genus Begomovirus. The first report of cassava mosaic disease (CMD) was from East Africa in 1894. Since then, epidemics have occurred throughout the African continent resulting in great economic loss and devastating famine. In 1971 a resistant line of cassava, the predominant host of this plant pathogenic virus, was established and used by the International Institute of Tropical Agriculture in Nigeria. This resistance worked as an effective control for many years. However, in the late 20th century, a more virulent virus broke out in Uganda and quickly spread to East and Central Africa. This highly virulent virus was later discovered to be a chimaera of two distinct begomovirus species.
Currently, CMD is managed through phytosantitation practices as well as the use of conventional resistance breeding. Additionally, vector management and cross-protection help to minimize transmission and symptom development. Though management practices are useful, the viruses’ high rate of recombination and co-infection capabilities have caused CMD to be one of the most detrimental diseases affecting food supply in Africa.
Hosts and symptoms[edit source | edit]
Cassava originated in South America and was introduced to Africa in relatively recent times. It is known to be a very drought-tolerant crop with the ability to yield even when planted in poor soils. When cassava was first grown in Africa, it was used for subsidiary purposes though it is now considered to be one of the most important food staple crops on the continent. Its production is moving toward an industrialized system in which plant material is used for a variety of products including starch, flour, and animal feed.
As cassava is vegetatively propagated, it is particularly vulnerable to viruses and thus Cassava geminiviruses lead to great economic loss each year. When these infect a host plant, the plant’s defense system is triggered. Plants use gene silencing to suppress viral replication, though begomoviruses have evolved a counter-acting suppressor protein against this natural host defense. Because different species of begomovirus produce different variants of this suppressor protein, co-infection by multiple species typically leads to more severe disease symptoms.
Initially following infection of a cassava geminivirus in cassava, systemic symptoms develop. These symptoms include chlorotic mosaic of the leaves, leaf distortion, and stunted growth. Infection can be overcome by the plant especially when a rapid onset of symptoms occurs. A slow onset of disease development usually correlates with death of the plant.
Though the cassava-infecting geminiviruses causes most of their economic damage in cassava, they are able to infect other plants. The host range depends on the species of virus and most are able to be transmitted and to cause disease on plants of the genera Nicotiana and Datura.
Causal agent and disease cycle[edit source | edit]
Cassava geminiviruses are transmitted in a persistent manner by the whitefly Bemisia tabaci, by vegetative propagation using cuttings from infected plants, and occasionally by mechanical means. Cassava produces its first leaves within 2-3 weeks of planting; these young leaves are then colonized by the viruliferious whiteflies. This is the key infection period for CMD geminiviruses, as they cannot infect older plants. As the genome of the viruses has two components, DNA A and B, that are encapsidated in separate geminate particles, it requires a double inoculation to cause infection.
Generally, whitefly requires 3 hours feeding time to acquire the virus, a latent period of 8 hours, after which it needs 10 minutes to infect the young leaves. There is variation in the literature on this score, however, with other sources citing a 4-hour acquisition time and 4-hour latent period. Symptoms appear after a 3-5 week latent period. Adult whiteflies can continue to infect healthy plants 48 hours after initial acquisition of the virus. A single whitefly is sufficient to infect the host; however, successful transmission increases when multiple infected whiteflies feed on the plant.
After entering the plant through the leaves, the virus remains in the leaf cells for 8 days. As it is a single-stranded DNA virus, it needs to enter the nucleus of the leaf cells to replicate. After this initial period, the virus enters the phloem and travels to the base of the stem and out into the branches. Travel to the branches of the plant is much slower than travel through the stem, so cuttings of branches from infected stems may be free of disease. Some literature has indicated that infection is limited to above-ground tissue, but it is not clear why this would be the case.
Environment[edit source | edit]
The severity of cassava mosaic disease is impacted by environmental factors such as light intensity, wind, rainfall, plant density and temperature. Given that the viruses are transmitted by whitefly, the spread of the virus is going to depend largely on the vector. Temperature is the most important environmental factor controlling the size of the vector population. In the literature, vector-preferred temperature estimates vary from 20°C to 30°C to 27°C to 32°C but generally high temperatures associated with high fecundity, rapid development, and greater longevity in whitefly. Increased light intensity has been shown to increase activity of the whitefly vector.
Whiteflies can fly at speeds up to 0.2 mph, and in high-wind conditions they can move much greater distances in a shorter time, thus increasing rate of virus spread. This wind-dependent spread is reflected in the location of the whitefly in cassava fields, with populations greatest in upwind boarders and lowest within the field.
Virus incidence increases when cassava is growing vigorously. Thus, plant density impacts the spread of the virus, with low-density fields encouraging faster disease propagation than high-density ones. In dry areas, rainfall can be a limiting factor for cassava growth so higher rainfall will be associated with higher incidence of disease. Populations of whitefly will increase with rainfall, but heavy rains may impede whitefly spread and thus decrease incidence of virus.
Timing of planting can play an important role in the severity of disease, with cassava planted in March showing a 74% incidence rate of CMV, compared with 4% in August. Seasonal distribution of the virus will vary with the climate. In tropical rain forest type climates, where it is wet and humid most of the year, rapid virus distribution occurred from November to June, and slow progress occurred from July to September. This timing correlated with higher and lower temperatures. In a study of the disease in the Ivory Coast of Africa, maximum rate of disease spread was reached two months after planting. Little to no infection occurs after three months, and variation in spread was due to change in temperature, radiation and population levels of whitefly.
Control strategies[edit source | edit]
Control strategies for cassava mosaic disease include sanitation and plant resistance. In this case, sanitation means using cuttings from healthy plants to start with a healthy plot and maintaining that healthy plot by identifying unhealthy plants and immediately removing them. This strategy does not protect them from being inoculated by whiteflies, but research shows that the virus is more aggressive in plants infected from contaminated cuttings than by insect vectors. There are also specific varieties that fare better against some viruses than others, so plant resistance is possible. For example, hybrids that are a result of crossing cassava and other species, such as Manihot melanobasis and M. glaziovii, have been shown to have considerable resistance to CMV.
Importance[edit source | edit]
Mostly grown as a food source in Africa, cassava is the third largest source of carbohydrates in the world. In recent times, cassava production has turned from subsistence to commercial production.
CMD was first described in 1894 and is now considered one of the most damaging crop viruses in the world. Annual economic losses in East and Central Africa are estimated to be between US$1.9 billion and $2.7 billion. Although cassava is also cultivated in Latin America and South East Asia, the geminiviruses infecting it are only found in Africa and the Indian sub-continent. This has been mainly attributed to the inability of B. tabaci to colonize cassava effectively in this part of the world.
References[edit source | edit]
- Patil B & Fauquet C (2009). Cassava mosaic geminiviruses: actual knowledge and perspectives. Molecular Plant Pathology. 10: 685–701.
- Legg J & Fauquet C (2004). Cassava mosaic geminiviruses in Africa. Plant Molecular Biology. 56: 585–599.
- Thresh J (2006). Control of tropical plant virus diseases. Virus Research. 67:245–295.
- Harrison B & Robinson D (1999). Natural genomic and antigenic variation in whitefly-transmitted geminiviruses (begomoviruses). Annual Review of Phytopathology. 37: 369–398.
- Legg J & Thresh J (2000). Cassava mosaic virus disease in East Africa: a dynamic disease in a changing environment. Virus Research. 71: 135–149.
- Bock K & Woods R (1983). The etiology of African cassava mosaic disease. Plant Dis. 67: 994–995.
- Timmermans, M.C.P., Das, O.P., Messing, J. (1994). Geminivurses and Their Uses as Extrachromosomal Replicons. Annu. Rev. Plant. Physiol. Plant. Mol. Biol. 45:79–112.
- Fargette, D. and Thresh, J.M. (1994). The Ecology of African Cassava Mosaic Geminivirus. In: Bakeman, J.P., Williamson, B. (Eds). Ecology of Plant Pathogens, CABI.
- Thurston, H.D. Tropical Plant Diseases. St. Paul: APS press, 1998.
- Fargette, D., Jeger, M., Fauquet, C., Fishpool, L.D. (1994). Analysis of Temporal Disease Progress of African Cassava Mosaic Virus. Phytopathology. 54; 1 91–98.
- Fauquet, C. and Fargette, D. (1990) African Cassava Mosaic Virus: Etiology, Epidemiology, and Control. Laboratoire de Phytovirologie, ORSTOM, Abidjan, Ivory Coast. Plant Disease. 74: 404-411.
- Thresh, JM & Cooter, T.J. (2005). Strategies for controlling Cassava Mosaic Disease in Africa. Plant Pathology. 54: 587–614.
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