Wheat streak mosaic virus (wheat streak)
- Summary of Invasiveness
- Taxonomic Tree
- Notes on Taxonomy and Nomenclature
- Distribution Table
- History of Introduction and Spread
- Risk of Introduction
- Habitat List
- Hosts/Species Affected
- Growth Stages
- List of Symptoms/Signs
- Biology and Ecology
- Means of Movement and Dispersal
- Seedborne Aspects
- Vectors and Intermediate Hosts
- Impact Summary
- Economic Impact
- Environmental Impact
- Impact: Biodiversity
- Social Impact
- Risk and Impact Factors
- Detection and Inspection
- Similarities to Other Species/Conditions
- Prevention and Control
- Gaps in Knowledge/Research Needs
- Links to Websites
- Distribution Maps
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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- Wheat streak mosaic virus
Preferred Common Name
- wheat streak
Other Scientific Names
- wheat streak mosaic potyvirus
- wheat streak mosaic rymovirus
International Common Names
- English: streak mosaic
Local Common Names
- Germany: Strichelmosaik-Virus des Weizens
- Italy: mosaico striato del frumento
- UK/England and Wales: wheat streak mosaic disease
Summary of InvasivenessTop of page
WSMV is an obligate parasite which infects wheat and other cereal crops and causes significant losses in production throughout many regions of the world. It is not listed as an invasive species, but introduction of the virus to other regions is possible due to a low occurrence of seed transmission. It is believed that WSMV entered the USA in the late 1800s (Reitz and Heyne, 1944; Ross, 1969) from Turkey and then moved into Canada and down into the southern states of the Great Plains as well as Mexico (Sanchez-Sanchez et al., 2001). The introduction of WSMV into Argentina and Australia is reported to be due to infected seed from both Mexico and the USA (Dwyer et al., 2007). Wheat streak is now commonly found throughout many countries and is one of the most common wheat viruses throughout the Central and Western Great Plains of the USA (Burrows et al., 2009).
Taxonomic TreeTop of page
- Domain: Virus
- Unknown: "Positive sense ssRNA viruses"
- Unknown: "RNA viruses"
- Family: Potyviridae
- Genus: Tritimovirus
- Species: Wheat streak mosaic virus
Notes on Taxonomy and NomenclatureTop of page
Wheat streak mosaic disease, caused by Wheat streak mosaic virus, was first identified in 1937 (McKinney, 1937). Wheat streak mosaic virus is a member of the Potyviridae virus family and is characterized as a single-stranded, filamentous RNA virus containing approximately 9383-9339 nucleotides (Stenger et al., 1998). The virus sequence contains a 130-nt 5' leader sequence and a 3' polyadenylated tail with a 149-nt 3' untranslated region. Genome organization shares the typical arrangement of the Potyviridae family (5'-P1/HC-Pro/P3/6K1/CI/6K2/VPg-NIa/Nib/CP-3') and codes for a 3035 amino acid single polyprotein. Wheat streak mosaic virus was originally a member of the Rymovirus genus until 1998 when it was placed in the Tritimovirus genus, due to differences in protein structure (Stenger et al., 1998).
DistributionTop of page
WSMV is found throughout wheat-growing regions of the world. It has been reported in the six continents. It is hypothesized (McNeil et al., 1996) that WSMV in the American Great Plains may constitute its own population separate from Eurasian isolates. The US isolates were found to be more closely related to Turkish isolates of WSMV than to other Eurasian isolates. These results suggest that the US and Turkish isolates diverged only recently when compared to the isolates from Mexico, central Europe, Russia and Iran. The three main isolates of WSMV found in North America are the Type, Sidney 81 and El Batán isolates (Stenger et al., 2002). The Type and Sidney 81 isolates are very similar and have 97.6% sequence identity (Choi et al., 2001). A large amount of divergence was found when the Type and El Batán isolates were compared. The differences between the Type, Sidney 81 and the El Batán isolates are thought to be due to genetic drift (Choi et al., 2001; Rabenstein et al., 2002). The El Batán isolate contains a 45 nt deletion and is believed to have been genetically isolated from the Great Plains populations much earlier (Choi et al., 2001). The common ancestry of the North American isolates with the Turkish isolates could suggest that the virus moved into the northern region of the US and then become separated from isolates that expanded into Mexico (Choi et al., 2001; Rabenstein et al., 2002). Studies by Rabenstein et al. (2002) determined that the isolates from Europe and Russia share the most recent common ancestry and represent a third population separate from the Asia Minor WSMV population. World isolates of WSMV are similar except for small deletions and insertions but contain a highly conserved coat protein region.
All isolates of WSMV have a highly conserved region containing 1267 nt which codes for the coat protein cistron and flanking sequences. This conserved region has been used to group the different isolates of the virus from many countries into groups of divergences or Clades (Stenger et al., 2002). Studies by Stenger et al. (2002) and Rabenstein et al. (2002) determined that WSMV isolates could be separated into four different clades (A-D) by nucleotide sequence comparison: Clade A from Mexico which contains the El Batán isolate; Clade B from Europe and Russia; Clade C from Iran; and Clade D which contains the US isolates, one from Canada and two Turkish isolates. Again a close relationship was found between the Turkish and US isolates suggesting recent movement between continents (Rabenstein et al., 2002; Stenger et al., 2002). Clade D of the US can be further sub-divided into subclades D1-4. Subclade D1 includes three isolates of the Pacific Northwest and an isolate for Washington. Subclade D2 contains six isolates from Kansas and Colorado and contains the subtype Type isolate of WSMV collected by HH McKinney (McKinney, 1937) and described by Brakke (1971). Subclade D2 also contains isolates isolated from Oklahoma and Ohio (Stenger et al., 2002). Subclade D3 contains isolates from Kansas, Missouri, Kentucky and Ohio, while the D4 subclade contains the Sidney 81 isolate from Nebraska and two isolates from Kansas. Today WSMV is the most common wheat virus found throughout the Great Plains region of the USA and causes substantial losses of up to 100% (Burrows et al., 2009).
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|China||Present||Introduced||Xie et al., 1982; CABI/EPPO, 2005|
|Iran||Present||Native||Foulad and Izadpanah, 1986; Stenger et al., 2002; CABI/EPPO, 2005|
|Jordan||Present||Introduced||SLYKHUIS and BELL, 1963; CABI/EPPO, 2005|
|Kazakhstan||Present||Introduced||Djiemboev, 1956; CABI/EPPO, 2005|
|Syria||Present||Introduced||Makkouk and Kumari, 1997, publ. 1998; CABI/EPPO, 2005|
|Turkey||Present||Native||Not invasive||Bremer, 1971; Stenger et al., 2002; CABI/EPPO, 2005|
|Zambia||Present||Introduced||Not invasive||Kapooria and Ndunguru, 2004|
|Canada||Present||Introduced||Not invasive||Stenger et al., 2002; CABI/EPPO, 2005|
|Mexico||Present||Introduced||Not invasive||Sanchez-Sanchez et al., 2001; Sánchez-Sánchez et al., 2001; CABI/EPPO, 2005|
|-Arkansas||Present||CABI/EPPO, 2005; Byamulama et al., 2013|
|-California||Widespread||Introduced||Not invasive||Jepson et al., 1975|
|-Colorado||Widespread||Introduced||Not invasive||Shahwan and Hill, 1984; CABI/EPPO, 2005; Byamukama et al., 2013|
|-Idaho||Widespread||Introduced||Not invasive||Stenger et al., 2002; CABI/EPPO, 2005|
|-Kansas||Widespread||Introduced||Not invasive||Christian and Willis, 1993; CABI/EPPO, 2005|
|-Kentucky||Widespread||Introduced||Not invasive||Stenger et al., 2002; CABI/EPPO, 2005|
|-Missouri||Widespread||Introduced||Not invasive||Stenger et al., 2002; CABI/EPPO, 2005|
|-Montana||Widespread||Introduced||Not invasive||CABI/EPPO, 2005; Burrows et al., 2009|
|-Nebraska||Widespread||Introduced||Not invasive||CABI/EPPO, 2005; Burrows et al., 2009; Byamukama et al., 2013|
|-New York||Present||CABI/EPPO, 2005|
|-North Dakota||Widespread||Introduced||Not invasive||TIMIAN and BISSONNETTE, 1964; CABI/EPPO, 2005|
|-Ohio||Widespread||Introduced||Not invasive||Stenger et al., 2002; CABI/EPPO, 2005|
|-Oklahoma||Widespread||Introduced||Not invasive||CABI/EPPO, 2005; Burrows et al., 2009|
|-South Dakota||Present||CABI/EPPO, 2005; Burrows et al., 2009; Byamukama et al., 2013|
|-Texas||Widespread||Introduced||Not invasive||CABI/EPPO, 2005; Burrows et al., 2009|
|-Washington||Widespread||Introduced||Not invasive||Stenger et al., 2002; CABI/EPPO, 2005|
|-Wyoming||Widespread||Introduced||Not invasive||CABI/EPPO, 2005; Burrows et al., 2009|
|Brazil||Present||Introduced||Not invasive||Mar et al., 2013|
|Czech Republic||Present||Introduced||Not invasive||Stenger et al., 2002|
|Germany||Present||Introduced||Not invasive||Chen et al., 2001|
|Hungary||Present||Introduced||Not invasive||Nyitrai and Gáborjányi, 1988; Stenger et al., 2002; CABI/EPPO, 2005|
|Italy||Present||Credi et al., 1997; CABI/EPPO, 2005|
|Poland||Present||Introduced||Not invasive||Jezewska and Wieczorek, 1998; CABI/EPPO, 2005|
|Russian Federation||Present||Introduced||Not invasive||Stenger et al., 2002; CABI/EPPO, 2005|
|-Southern Russia||Present||CABI/EPPO, 2005|
|Ukraine||Present||Native||Not invasive||Reshetnik et al., 1996; CABI/EPPO, 2005|
|Yugoslavia (former)||Present||Native||Not invasive||Juretic, 1979|
|Yugoslavia (Serbia and Montenegro)||Present||CABI/EPPO, 2005|
|-New South Wales||Present||CABI/EPPO, 2005; Milgate et al., 2016|
|-Queensland||Present||Introduced||Not invasive||CABI/EPPO, 2005; QPIF, 2012|
|-South Australia||Present||CABI/EPPO, 2005|
|New Zealand||Widespread||Introduced||Not invasive||Lebas et al., 2009|
History of Introduction and SpreadTop of page
WSMV is commonly found throughout the majority of wheat-growing regions worldwide. It is believed that WSMV was introduced into North America due to human immigration from Crimea along with the movement of hard red winter wheat into South Dakota, Nebraska and Kansas during the 1880s (Reitz and Heyne, 1944; Ross, 1969). Studies have shown a low occurrence of seed transmission of WSMV in wheat and maize lines, which could be a possible route for virus introduction (Hill et al., 1974). After introduction into the USA, WSMV spread throughout the Great Plains and has also been identified in Canada and Mexico (Sanchez-Sanchez et al., 2001; Rabenstein et al., 2002). The exact origin of WSMV is unknown, but it is thought that it could have originated in northern Europe and then moved south into areas of Asia, and into North America.
IntroductionsTop of page
|Introduced to||Introduced from||Year||Reason||Introduced by||Established in wild through||References||Notes|
|Natural reproduction||Continuous restocking|
|Argentina||USA||2002||Crop production (pathway cause)||Yes||No||Stenger and French (2009)||Accidental|
|Australia||Mexico||2007||Crop production (pathway cause)||Yes||No||Dwyer et al. (2007)||Accidental|
|USA||Krymskaya Oblast||1800s||Crop production (pathway cause)||Yes||No||Reitz and Heyne (1944)||Accidental|
Risk of IntroductionTop of page
WSMV is endemic to many wheat-growing regions. It is the most common wheat virus affecting the Central and Western Great Plains region of the USA (Burrows et al., 2009; Byamukama et al., 2013) and many other countries (Stenger et al., 2002). WSMV was isolated from wheat in Xinjiang in 1982 (Xie et al., 1982). The virus and its vector, Aceria tosichella, were then found infecting several varieties of winter wheat in Poland (Jezewska and Wieczorek, 1998; Kozlowski, 2000). In 2002 WSMV was discovered in Argentina (Truol et al., 2004) and was determined to be closely related to isolates from the American Pacific Northwest and Australia. It is possible that the two introductions were from the same source and that this particular lineage of WSMV is seedborne at a greater rate than other WSMV lineages (Stenger and French, 2009). The Australian isolate of WSMV was found in greenhouse-grown breeding lines from Centro Internacional de Mejoramiento de Maiz y Trigo (CIMMYT) in Mexico (Sanchez-Sanchez et al., 2001; Dwyer et al., 2007) and is seedborne at a rate of 0.5-2%, which is greater than previously reported (Hill et al., 1974). The differences between seed transmission rates for different WSMV isolates has not been fully explored and therefore it is still unknown the extent to which seed transmission plays a role in introduction of WSMV.
HabitatTop of page
WSMV is an agricultural pathogen and its presence is primarily noted in wheat production areas. No information is available on the impact of WSMV on other hosts.
Habitat ListTop of page
|Terrestrial – Managed||Cultivated / agricultural land||Present, no further details||Productive/non-natural|
|Protected agriculture (e.g. glasshouse production)||Secondary/tolerated habitat||Harmful (pest or invasive)|
|Managed grasslands (grazing systems)||Present, no further details||Natural|
|Industrial / intensive livestock production systems||Present, no further details||Natural|
|Urban / peri-urban areas||Present, no further details||Natural|
|Terrestrial ‑ Natural / Semi-natural||Natural grasslands||Present, no further details||Natural|
Hosts/Species AffectedTop of page
WSMV can infect a variety of agricultural crops including many species of wheat (Triticum spp.), oats, barley, triticale, millet, rye and maize, as well as a range of wild grasses including giant foxtail (Setaria faberi), prairie cupgrass (Eriochloa contracta), green foxtail (Setaria viridis), witchgrass (Panicum capillare), barnyard grass (Echinochloa crus-galli), cheatgrass (Bromus tectorum) and Kentucky bluegrass (Poa pratensis) (Brakke, 1971; Christian and Willis, 1993; Ito et al., 2012). Many of these grasses can serve as reservoir hosts for both the virus and the wheat curl mite vector (Aceria tosichella).
Growth StagesTop of page Seedling stage, Vegetative growing stage
SymptomsTop of page
Symptoms of wheat streak mosaic typically start at the edge of the field, with severe yellowing, and decrease in severity with distance into the field (Workneh et al., 2009a). This is due to the movement of the mite vector over time and subsequent disease spread. Infections stemming within the field are also common, where white curl mites move from volunteer wheat and grass weeds within the field (Byamukama et al., 2016). Infection by WSMV is not considered to be a latent infection and is characterized by stunting, reduction in tiller number, and chlorosis or the breakdown of chlorophyll within the plant leaves progressing to a mosaic pattern and streaking appearance, which eventually leads to necrosis and severe stunting (Wiese, 1987). More severe symptoms are found when wheat becomes infected in the autumn and under mild winter conditions compared to wheat infected in the spring or summer, which could be due to plant age at the time of infection (Hunger et al., 1992). During severe infections, the wheat heads do not produce grain, especially on the side tiller, or contain non-viable, small, shrivelled seeds.
List of Symptoms/SignsTop of page
|Growing point / dwarfing; stunting|
|Inflorescence / dwarfing; stunting|
|Inflorescence / mosaic|
|Leaves / abnormal colours|
|Leaves / abnormal patterns|
|Leaves / necrotic areas|
|Leaves / yellowed or dead|
|Roots / reduced root system|
|Seeds / empty grains|
|Seeds / shrivelled|
|Whole plant / discoloration|
|Whole plant / dwarfing|
|Whole plant / early senescence|
|Whole plant / plant dead; dieback|
Biology and EcologyTop of page
WSMV can survive in a variety of environments as long as a primary or alternative host and the mite vector (Aceria tosichella) are present. It is an obligate parasite and must have a viable host for replication. The virus relies exclusively on its vector for transfer from host to host (Slykhuis, 1955) and survives in non-wheat production areas by using alternative hosts such as a variety of native grasses (Bowden et al., 1991; Christian and Willis, 1993). WSMV can also survive in seed and be transmitted to the seedling but seed transmission rates are very low (Jones et al., 2005)
Means of Movement and DispersalTop of page
Vector transmission (biotic)
WSMV is vectored by the wheat curl mite (Aceria tosichella) (Slykhuis, 1955; Keifer, 1969). A tosichella is a member of the family Eriophyidae and is a soft-bodied, white, spindle-shaped mite measuring from 210 to 250 µm long (Keifer et al., 1982). Their microscopic size makes scouting for infestations in agricultural fields difficult because they can only be viewed under a stereoscope at 30 to 40X magnification, or with the use of a 20x hand lens. Typically volunteer wheat serves as the main host to the wheat curl mite and WSMV during summer (Shahwan and Hill, 1984); however, there are a variety of native grasses that can serve as alternative hosts for both the wheat curl mite and the virus. Hosts for the wheat curl mite include jointed goatgrass (Aegilops cylindrica), western wheat grass (Elymus smithii), grama (Bouteloua sp.), sandbur (Cenchrus incertus), smooth crabgrass (Digitaria ischaemum), Canada wild-rye (Elymus canadensis) and Johnson grass (Sorghum halepense) (Connin, 1956). These primary and alternative hosts serve as a 'green bridge' for infestation and infection by the mite and virus in autumn-planted wheat production fields (Bowden et al., 1991; Christian and Willis, 1993). Mites are carried from these reservoir areas by winds and typically build in population on the edge of the field. These mites then move inward with the wind, spreading infection and creating a disease gradient with severe disease on the edge of the field and decreases in severity with distance into the field (Workneh et al., 2009a). Sometimes WSMV can be spread from volunteer wheat and grassy weeds within the field, in which case, the entire field can be infected with WSMV without the display of an obvious gradient (Byamukama et al., 2016).
Seedborne AspectsTop of page
WSMV is seed transmitted at very low frequencies of 0.5 to 1.5% in eight different wheat genotypes (Jones et al., 2005). It is believed that the introductions of WSMV into both Argentina and Australia could have been due to infected seed that was imported into the country from the USA and Mexico (Stenger and French, 2009). The WSMV isolate that was discovered in Australia was found in greenhouse-grown breeding lines from Centro Internacianal de Mejoramiento de Maiz y Trigo (CIMMYT) in Mexico (Sanchez-Sanchez et al., 2001; Dwyer et al., 2007). Australian isolates of WSMV were seedborne at a rate of 0.5-2%, which is greater than previously reported (Hill et al., 1974; Stenger and French, 2009). It is possible that the introduction of WSMV into the USA was also from an infected seed source (Reitz and Heyne, 1944; Ross, 1969). However, the rates of seed transmission of many of the WSMV isolates are extremely low or still need to be examined to evaluate its true potential as a source of introduction.
Effect on Seed Quality
WSMV causes reductions in yield and also seed weight. Seeds from infected plants typically appear shrivelled and have a lower seed weight than seed from healthy plants (Hunger, 1992). No data are available on germination or vigour.
There are no seed treatments available that will help against seedborne infection of WSMV.
Vectors and Intermediate HostsTop of page
Impact SummaryTop of page
Economic ImpactTop of page
Losses due to WSMV have been recorded for many years throughout the world (Atkinson and Grant, 1967). In Australia during 2005 and 2006, WSMV caused crop failures of 5000 and 20,000 hectares, respectively (Cross, 2012). WSMV has been estimated to cause an average reduction in wheat yields of 2.6% per year in Kansas, USA (Christian and Willis, 1993). In 2017, WSMV was reported to cuase US$ 76.8 million in revenue losses in Kansas (Kansas Wheat Commission, 2017). However, losses can range from low to 100% depending on the time of infection and the wheat variety planted (Edwards and McMullen, 1987). During studies with 12 different varieties of winter wheat in Colorado, USA, reductions in grain yield due to WSMV infection ranged from 50 to 91% (Shahwan and Hill, 1984). Typically reductions due to WSMV are found to be more severe primarily during autumn infections; however, yield losses can be quite significant when wheat becomes infected in the early spring (Hunger et al., 1992; Hunger, 2004). Wheat streak mosaic not only affects grain yield but also root development and water use efficiency of infected wheat (Price et al., 2010a).
WSMV has also been found to cause significant damage to the root systems of infected plants. Root systems of diseased plants can be reduced by up to 50% or more due to infection (Price et al., 2010a). Byamukama et al. (2012) reported reduction in root mass of 27% in a susceptible cultivar when inoculated with WSMV relative to a non-inoculated control under greenhouse conditions. This reduction in root biomass causes a reduction in water uptake and water use efficiency in diseased fields. Studies by Price et al. (2010a) determined that plots inoculated in the autumn with WSMV had significantly more soil moisture left in the soil profile due to the reductions in root biomass. Therefore, diseased root systems were not able to take up available soil moisture as efficiently as healthy plants. This is particularly important in areas with dry climates that are highly dependent on irrigation. Economic evaluations were assessed using the recorded reductions in wheat yield during the study by Price et al. (2010a) to evaluate overall losses due to WSMV in both irrigated and non-irrigated systems (Velandia et al., 2010). Calculation of marginal losses due to WSMV infection included not only grain yield but also reductions in forage and the cost of irrigation. It was determined that overall losses were greater for irrigated treatments due to the additional cost of pumping fees. Overall losses increased four-fold. or by 293%, when comparing the marginal losses of fully irrigated to dryland production due to WSMV infection. Losses were estimated to be US $464.5/ha for the full irrigation treatment (Velandia et al., 2010). Similar results were found when examining disease severity gradients created by the movement of the wheat curl mite vector, Aceria tosichella, into infected fields. A positive linear relationship between disease severity and soil moisture was found indicating that severely diseased areas of a field had greater soil water content than less severe or healthy areas of the field (Workneh et al., 2009b). Significant losses in grain yield were found with increased disease severity up to 150 m into the infected field, therefore the application of site-specific irrigation during times of disease could be used as a possible management strategy.
WSMV also commonly occurs in complex with wheat viruses: Triticum mosaic virus (TriMV) and High Plains wheat mosaic virus (Burrows et al., 2009; Byamukama et al., 2013). The three viruses are transmitted by the same vector, wheat curl mites and are found throughout the wheat-growing region of the USA. During co-infection by WSMV and TriMV a disease synergism is induced causing an increase in disease severity (Tatineni et al., 2010). Grain yield loss from plots inoculated with WSMV and TriMV was reduced by 96% in a susceptible cultivar compared to a non-inoculated control (Byamukama et al., 2014). Identification of the causal pathogen is therefore very important for management.
Environmental ImpactTop of page
WSMV negatively affects water use efficiency and may lead to water wastage in irrigated fields. Severe WSMV leads to stunting of plants which may lead to weeds developing due to reduced competition from wheat.
Impact: BiodiversityTop of page
Several grass species are susceptible to WSMV. In areas where this virus may be introduced, the susceptible native grass species could be lost due to competition from non susceptible species.
Social ImpactTop of page
WSMV development in larger portions of the field can lead to total loss of the crop, where the whole field is planted into another crop or left unharvested due to stuntedness. Yield loss due to WSMV could result in unstable food supply and high food prices.
Risk and Impact FactorsTop of page Invasiveness
- Has a broad native range
- Has high genetic variability
- Changed gene pool/ selective loss of genotypes
- Host damage
- Modification of nutrient regime
- Negatively impacts agriculture
- Negatively impacts livelihoods
- Difficult to identify/detect in the field
- Difficult/costly to control
DiagnosisTop of page
Most of the viruses infecting wheat cause similar symptoms as WSMV. Moreover, other diseases and stresses may elecit similar symptoms. WSMV can only be differentiated from other viruses through the use of serological testing such as an enzyme-linked immunosorbent assay (ELISA)(Seifers et al., 2006) or through molecular testing by polymerase chain reaction (PCR) (French and Robertson, 1993; Price et al., 2010b). Serological testing materials can be obtained through commercial testing suppliers. Information on testing services for producers can be located by contacting local Agricultural Extension Services and universities. Many American universities have a Plant Pathology Diagnostics laboratory that can perform pathogen testing on a variety of different crops. In the USA, the National Plant Diagnostics Network (NPDN; http://www.npdn.org/) is a nationwide plant disease monitoring network that deals with all types of plant diseases and can provide useful information on testing and identification. Commercially available ELISA kits can be purchased from Agdia (Agdia.com) or AC Diagnostics and other providers..
Detection and InspectionTop of page
Symptoms of WSMV can be identified by visual observation for chlorosis in leaf tissues. However, there are other pathogens that cause symptoms identical to WSMV therefore identification by molecular or serological testing is needed for WSMV confirmation (see Diagnosis). Plants suspected to be infected with WSMV are examined for chlorosis of leaf material and stunting of individual plants either late in the autumn or during the spring and summer. Typically, in more northern states of the USA, symptoms will not be obvious until late spring or early summer, whereas in southern regions of the USA, where temperatures remain relatively warm in autumn, it is sometimes possible to see symptom development in late autumn and early spring, depending on the time of infection. New techniques are being explored for detection of WSMV infections using remote sensing and satellite imagery. Studies by Mirik et al. (2011) demonstrated the ability to identify and calculate the percentage of fields infected by WSMV using Landsat 5 Thematic Mapper (TM) satellite images. Accuracy assessments for the presence and absence of WSMV were between 89.47 and 99.07% during large-area wheat monitoring of two counties in the Texas Panhandle during the 2005-2006 and 2007-2008 crop years.
Similarities to Other Species/ConditionsTop of page
Infection by WSMV is very similar to other viruses found throughout the Great Plains region of the USA. Disease symptoms are characterized by a reduction in chlorophyll content within infected plants leading to a mosaic streaking pattern, which eventually leads to stunting, necrosis and premature leaf senescence (Wiese, 1987). Similar viruses include Barley yellow dwarf virus (BYDV), Cereal yellow dwarf virus (CYDV) andSoil-borne wheat mosaic virus (SBWMV). These pathogens induce similar symptoms of chlorosis and stunting that is commonly found with WSMV; however, BYDV and CYDV are aphid transmitted (D’Arcy and Domier, 2000) and SBWMV is transmitted by the soilborne fungus Polymyxa graminis (Cadle-Davidson and Gray, 2006). These viruses are not mechanically transmitted, unlike WSMV. Two other very important viruses that are identical to WSMV areTriticum mosaic virus (TriMV) (Seifers et al., 2008) and High Plains wheat mosaic virus (HPWMoV), formerly High Plains virus (Jensen et al., 1996; Skare et al., 2006). These viruses display identical symptoms to WSMV and share the same vector (Aceria tosichella) as WSMV (Keifer, 1969; Seifers et al., 1997). These pathogens are commonly found together as co-infections within the same plant, particularly WSMV and TriMV (Burrows et al., 2009; Barumakama et al., 2013). These three pathogens cause identical symptoms and can only be differentiated from one another by the use of either serological or molecular tests.
Prevention and ControlTop of page
Due to the variable regulations around (de)registration of pesticides, your national list of registered pesticides or relevant authority should be consulted to determine which products are legally allowed for use in your country when considering chemical control. Pesticides should always be used in a lawful manner, consistent with the product's label.
WSMV can be prevented from introduction into new areas by ensuring the exchange or purchase of seed for planting is free of the virus. Seed for planting should come from disease-free areas. Once WSM is established in an area, it is not possible to eradicate it because it can survive on several wild grass species.
Management practices such as the elimination of volunteer wheat before planting wheat and late planting are currently the most reliable methods of disease control for WSMV. Volunteer wheat is the term used for wheat plants that germinate and survive between wheat summer and autumn. These plants serve as the primary reservoir for the pathogen and vector (Bowden et al., 1991). Volunteer wheat becomes a major reservoir for wheat viruses if there is a pre-harvest hail event. After wheat germination, the wheat curl mites are blown from volunteer wheat from neighbouring previous wheat fields into new production fields spreading the disease. Another method of WSMV control is late planting. Typically in the southern region of the Great Plains, wheat is planted in late August to early September for dual purpose of cattle grazing and grain. Early planting increases the chances of infection by WSMV, therefore late planting is suggested to decrease the likelihood of autumn infection. It has been found that planting late in September to early October will reduce the possibility of infection as well as disease severity (Hunger et al., 1992). However, the early planting strategy for WSMV control may be region specific and may not be as effective due to warmer autumn temperatures in southern regions. The use of resistant cultivars such as Mace and RonL has also been explored for control of WSMV. These varieties contain WSM genes of resistance to WSMV; however, this resistance in RonL is temperature sensitive above 25-28°C (Seifers et al., 2006). There are no pesticides that are labelled for use against the wheat curl mite.
Gaps in Knowledge/Research NeedsTop of page
Little is known about the affects of environmental factors on the movement and disease spread of WSMV. Various alternative hosts have been identified, but the actual role that these hosts play in disease epidemiology is unknown. Research efforts should be initiated to determine the role that alternative hosts play in disease spread and the role that wheat environmental factors play in dispersal from these areas.
ReferencesTop of page
Atkinson TG, Grant MN, 1967. An evaluation of streak mosaic virus losses in winter wheat. Phytopathology, 57:188-192
Bowden RL, Brooks HL, Peterson DE, Shroyer JP, 1991. Be a good neighbor: Control your volunteer wheat. K-State Extension Publication MF-1004. Aug, No. MF-1004., USA: Kansas State University
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OrganizationsTop of page
USA: Kansas State University - Plant Pathology - KSU, 4024 Throckmoton Plant Sciences Center, Manhattan Ks 66506, http://www.plantpath.ksu.edu/
USA: Texas A&M AgriLife Reserch Center-Plant Pathology, 6500 Amarillo Blvd. W, Amarillo Texas 79106, http://amarillo.tamu.edu/
USA: United States Department of Agriculture USDA, http://www.usda.gov/wps/portal/usda/usdahome
USA: University of Nebraska-Lincoln-Plant Pathology, 406 Plant Science Hall, Lincoln NE 68583-0722, http://plantpathology.unl.edu/
ContributorsTop of page
26/09/17 Review by:
Emmanuel Byamukama, Agronomy, Horticulture & Plant Science, South Dakota State University, USA
21/11/12 Original text by:
Jacob Price, Senior Research Associate, Plant Pathology, Texas AgriLife Research, Amarillo, Texas, USA
Charlie Rush, Professor of Plant Pathology, Texas AgriLife Research, Amarillo, Texas, USA
Distribution MapsTop of page
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