Corn lethal necrosis -Maize lethal necrosis

​One of the more damaging virus diseases is caused by the combination of maize chlorotic mottle virus (MCMV) and any of the potyviruses maize dwarf mosaic virus (MDMV), wheat streak mosaic virus (WSMV) or sugarcane mosaic virus (SCMV).  First identified in Peru in 1972, in Kansas and Nebraska in 1982 and Argentina in 1983.  It was reported in China in 2010 and Kenya in 2011.

MCMV is transmitted by beetles, mainly Diabrotica species, and thrips (genus Frankliniella).  These vectors also feed on possible alternate grass hosts of this virus. The virus can be transmitted by the larvae of Diabrotica in the soil or adult root worm beetles.  MDMV RNA codes for the protein coat plus a few other proteins needed for replication but, like other plant viruses utilizes the host cytoplasm for materials and organelles to do the replication.  Unless infected before V4 stage, the plants will not show stunting or early death but will have chlorotic mottling in leaves. Later plant feeding by adult beetles results in early death of ear husk leaves and small ears.  In the USA, most severe damage because of early infection comes with continuous corn cropping and rootworm larvae.  This is usually (always?) includes infection by one of the other viruses that are transmitted by aphids (MDMV and SCMV) or wheat leaf curl mite (WSMV).  There is evidence of symptomless plants infected by MCMV if none of the other viruses are present.  It is possible that this virus has been present on maize and other related grasses worldwide but has only became noted when the combinations with the other viruses caused significant symptoms.

Severe damage does require the complex interacting biology of the vectors, other virus hosts and corn growth stage.  It needs to increase to a level that it can be noted in the field as well.  Susceptible genotypes appear to be much more frequent than resistant but, in each case of a new occurrence, a few years of searching successfully identified resistance genotypes.  This is consistent with our experience with several other known viruses infecting corn.  An apparently new occurrence, then an investigation of pathogens, followed by a survey of genotypes for resistance and an investigation for the dynamics of disease.  Eventually humans figure it out.  All is well until the next disease outbreak.  We should be thankful that the basic biology of that open pollinated species selected by humans was exposed to many environments resulting in large genetic variability.