Non-crop plants such as grasses and volunteer plants are an inseparable part of the flora of crop fields, and can influence virus incidence in crop plants. The presence of grasses as virus reservoirs can lead to a higher probability of virus incidence in crop plants. However, the role of reservoirs as an inoculum source in agricultural fields has not been well studied for many viral diseases of crops. Grasses have been found to constitute potential reservoirs for cereal-infecting viruses in different parts of the worlds. This study revealed that cereal-infecting viruses such as wheat dwarf virus (WDV), barley yellow dwarf viruses (BYDVs) and cereal yellow dwarf virus-RPV (CYDV-RPV) can be found among ryegrass growing in or around winter wheat fields. Phylogenetic analysis showed that a WDV isolate from ryegrass was a typical WDV-E isolate that infects wheat. Similarly, a ryegrass isolate of BYDV-PAV grouped in a clade together with other BYDV-PAV isolates. Inoculation experiments under greenhouse condition confirmed that annual ryegrass of various genotypes can be infected with WDV to a very low titre.Moreover, leafhoppers were able to acquire WDV from infected ryegrass plants, despite the low titre, and transmit the virus to wheat resulting in symptoms. Information from the grass reservoir may contribute to improving strategies for controlling plant virus outbreaks in the field. Knowledge of the likely levels of virus in potential reservoir plants can be used to inform the decisions on insect vector control strategies, and may help to prevent virus disease outbreaks in the future.
For pathogens infecting single host species evolutionary trade-offs have previously been demonstrated between pathogen-induced mortality rates and transmission rates. It remains unclear, however, how such trade-offs impact sub-lethal pathogen-inflicted damage, and whether these trade-offs even occur in broad host-range pathogens. Here, we examine changes over the past 110 years in symptoms induced in maize by the broad host-range pathogen, maize streak virus (MSV). Specifically, we use the quantified symptom intensities of cloned MSV isolates in differentially resistant maize genotypes to phylogenetically infer ancestral symptom intensities and check for phylogenetic signal associated with these symptom intensities. We show that whereas symptoms reflecting harm to the host have remained constant or decreased, there has been an increase in how extensively MSV colonizes the cells upon which transmission vectors feed. This demonstrates an evolutionary trade-off between amounts of pathogen-inflicted harm and how effectively viruses position themselves within plants to enable onward transmission.
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