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Symptoms in tomato (Lycopersicon esculentum) are greatly affected by temperature, day length, light intensity, age of plant when infected, virulence of infecting virus and cultivar (Hollings and Huttinga, 1976). However, infected greenhouse-grown tomatoes in summer develop light and dark green leaf mottling and, sometimes, distortion of young leaves. In winter, with short days, low light intensity and low temperatures (below 20°C), plants are often severely stunted. The laminae of leaves is much reduced ("fern-leaf") and yield is greatly reduced.
Some strains can cause more conspicuous symptoms such as yellow mottling of leaves and fruit (so-called aucuba symptoms), and others so-called "single virus streak" in which stems, petioles, leaves and/or fruit develop necrotic streaks. Others can cause internal necrosis or "bronzing" if plants are infected when fruits are developing, winter necrosis, summer necrosis or crusty fruit (Hollings and Huttinga, 1976).
ToMV and potato X potexvirus together cause dark brown and black stem streaking, a disease described as "double streak" (Broadbent, 1976).
Many Capsicum annuum cultivars are resistant to ToMV. However, in intolerant cultivars, the virus causes veinal and leaf necrosis, wilting and defoliation. Leaves developing subsequently on axillary shoots also usually develop conspicuous symptoms (see Miller and Thornberry, 1958).
ToMV causes severe leaf mottling and distortion in tobacco (Nicotiana tabacum) and potato (Solanum tuberosum), and stem necrosis and stunting in the latter (Komuro and Iwaki, 1968; Horvath et al., 1978; Juretic et al., 1978).
In Chenopodium murale, ToMV can cause severe leaf distortion, necrosis and stunting (Bald and Paulus, 1963).
ToMV induces no conspicuous symptoms in Syringa or Picea rubens (Jacobi and Castello, 1991a; Castello et al., 1992).
Use of Resistant Cultivars
Three major genes (designated Tm-1, Tm-2 and Tm-2²) for resistance have been most used in tomato breeding programmes. The earlier use of cultivars containing genes Tm-1 and/or Tm-2 resulted in the rapid emergence or increased incidence of strains which were able to overcome resistance (see Brunt, 1988). However, gene Tm-2² in homozygous cultivars, or together with genes Tm-1 and/or Tm-2, has been highly effective in controlling ToMV for two decades or so. Although the molecular basis for genetic resistance has yet to be determined, the genes probably inhibit virus multiplication and movement. The origin and exploitation of genes Tm-2 and Tm-2² have been fully reviewed by Hall (1980). Resistance to ToMV has also been reported in Capsicum annuum (Jilaveanu et al., 1984; Patagas et al., 1989).
Mild Strain Protection
Before genotypes with effective genetic resistance to ToMV became generally available, virus-induced losses were often reduced by prior infection of seedlings with a mild or attenuated strain of ToMV (Brunt, 1988). This procedure, although once widely used, is now unnecessary where resistant cultivars are grown.
Ideally, seed should only be collected from mother plants shown to be free of virus. Treatment of freshly harvested seed with dilute hydrochloric acid will inactivate virus contaminating seed coats. If the health status of seed is unknown, any virus on seed coats and in endosperm can also be eliminated by dry heating seed at 70°C for 2-4 days (Broadbent, 1965b; Laterrot and Pecaut, 1965). Externally located virus can be eliminated by soaking seed for 20 min in 10% (w/v) tri-sodium phosphate solution (Broadbent, 1976; Hollings and Huttinga, 1976).
The use of virus-free seed, the cultivation of plants in sterilised compost in plastic bags ('growbags') or hydroponic systems in which the nutrient solution is virus-free and application of strict hygiene can often reduce and sometimes prevent infection occurring (Broadbent, 1976). Tobacco in cigars, cigarettes and pipe tobacco was once thought to be an important source of ToMV. However, it is now recognized that, although tobacco might occasionally be such a source of infection of tobacco mosaic tobamovirus, it is very unlikely to be a source of ToMV (Broadbent, 1976). When infection is detected in a crop, milk sprays can minimise spread by inhibiting mechanical transfer of virus from infected to healthy plants (Crowley, 1958). It is also advisable that all tools be dipped in 3% (w/v) tri-sodium phosphate solution and that nursery workers thoroughly wash hands and any contaminated clothing (Broadbent, 1976).
Spread in crops grown in hydroponic systems can be prevented or minimized by pasteurization of the nutrient solution (Vetten, 1996).
Non-conventional resistance to ToMV has been conferred on genetically engineered plants containing the virus coat protein gene (Nejidat and Beachy, 1990; Yeh et al., 1996), antisense viral RNA and a ribozyme (Feyter et al., 1996). Such procedures have great potential for future use, but they have not yet been used experimentally.
Two proteins identified as host factors, TOM1 and TOM3, supported virus multiplication in N. tabacum. Silencing of these two genes by RNAi approach successfully inhibited the spread of tobamovirus (Asano et al., 2005). A plant integral membrane protein TOM1 is involved in the multiplication of Tomato mosaic virus (ToMV). TOM1 interacts with ToMV replication proteins and has been suggested to tether the replication proteins to the membranes where the viral RNA synthesis takes place. Inactivation of TOM1 results in reduced ToMV multiplication (Hagiwara-Komoda et al., 2008).
It has been estimated that ca 20% of the world's production of greenhouse-grown tomatoes was formerly lost due to infection by ToMV (Broadbent, 1976). However, the virus became much less important, especially in greenhouse-grown crops, after the introduction of resistant cultivars (especially those containing the Tm 2² gene) ca 20 years ago (Hall, 1980). Nevertheless, the yield of infected non-resistant greenhouse- or field-grown susceptible crops can be reduced by up to 25% (Weber, 1960; Crill et al., 1973; Brisson et al., 1984; Hervert and Hanusova, 1986; di Candilo et al., 1992).