Wheat streak mosaic virus
(wheat streak)

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).

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).

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. 

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.

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).

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)

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. 

Seed treatments

There are no seed treatments available that will help against seedborne infection of WSMV.

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..

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.

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.

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.

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.

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/

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