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For field-grown maize infected with MCMV, growth is stunted with the formation of short internodes. Leaf symptoms begin as chlorotic stripes running parallel to the veins which later coalesce to produce elongated chlorotic blotches, finally resulting in leaf necrosis and epinasty. In severe infections of particularly susceptible lines, leaf necrosis can result in plant death (Castillo and Hebert, 1974). Male inflorescences have hard panicles, short rachis and few spikelets. Fewer ears and ear malformation can also occur in severe infections (Castillo, 1976). A general observation is that the younger the maize plant is when MCMV infects, the more severe the stunting and symptoms become (Lenardon et al., 1987).
MCMV has been detected by serological methods in all parts of an infected maize plant, including leaf, stem, roots, cob, husk, silk, kernel, seed, anther and sheath tissues (Jiang et al., 1992).
When MCMV co-infects maize with any potyvirus, a synergistic interaction occurs, causing a severe disease called corn lethal necrosis (CLN) (Niblett and Claflin, 1978). In maize the most common potyviruses found in co-infections with MCMV are maize dwarf mosaic potyvirus (MDMV) A and/or B. The symptoms of corn lethal necrosis are much more severe than the additive symptoms of either MCMV or the potyvirus virus alone. The virus complex causes a severe systemic necrosis which culminates in death of the plant (Niblett and Claflin, 1978; Uyemoto et al., 1980; Uyemoto et al., 1981). If maize plants exhibit a rapid onset of necrosis followed by rapid plant death, it is likely that they are infected with both MCMV and a maize-infecting potyvirus. The titre of MCMV in plants infected with both MCMV and a potyvirus is more than five times higher than in plants infected with MCMV alone (Goldberg and Brakke, 1987). From an epidemiological perspective, corn lethal necrosis can occur wherever both MCMV and a maize infecting potyvirus are endemic.
The most effective control for MCMV will be the deployment of resistant varieties. A number of sources of resistance to MCMV have been identified and are being incorporated into commercial maize varieties throughout the Western Hemisphere (Nault and Findley, 1981; Nault et al., 1982). Alternatively, crop rotation with sorghum or another non-maize crop has been shown to reduce the incidence of MCMV the following year (Phillips et al., 1982; Uyemoto, 1983). Soil fumigation apparently does not control MCMV.
Corn lethal necrosis, the disease caused by the synergistic interaction between MCMV and a maize-infecting potyvirus, can be controlled by effectively controlling and eliminating the infection of either component virus. Corn lethal necrosis has been controlled experimentally using transgenic resistance derived from a pathogen (Murry et al., 1993). Transgenic maize plants expressing the MDMV strain B capsid protein did not lead to corn lethal necrosis when inoculated with MDMV and MCMV.
In Peru, losses in floury and sweet maize varieties due to MCMV have been reported to average between 10 and 15%. In experimental plots, inoculated plant yields were reduced by up to 59% (Castillo, 1976). In Kansas crop losses due to corn lethal necrosis (caused by MCMV and any potyvirus) have been estimated to be between 50 (Uyemoto et al., 1980) and 90% (Niblett and Claflin, 1978) depending on the variety of maize and the year.