Changes in the Genetic Structure of Beet Necrotic Yellow Vein Virus Populations Associated with Plant Resistance Breakdown

The genome of BNYVV consists of 4 to 5 single-stranded, RNA particles. RNA 1 and 2 encode the essential elements for virus replication, protein encapsidation, and cellular translocation, whereas RNA 3, 4, and 5 are involved in disease expression and vector transmission. Despite its multi-partite genome, and the potential of mixed infections with BSBMV, high genetic stability seems to be the norm. These observations suggest the existence of strong selective constraints on virus diversification, and effective isolation mechanisms operating among populations of BNYVV. When a plant is infected by BNYVV, it is actually infected by a large collection of virus particles that are closely related, but not identical to each other. The specific molecular composition of these particles is referred to as virus population structure. Usually, when a virus is isolated from an infected plant, the virus is defined by the “average” genetic structure of all the infecting particles, and genetic variability of the virus population is not considered. However, when an infecting viral population whose specific genetic structure, rather than its average or dominant genotype, is discussed, it is referred to as a quasispecies. Few studies have investigated the quasispecies structure of plant viruses, even though it is likely that the quasispecies structure is the most important descriptive attribute of any specific virus isolate. In general, most infecting viral populations are composed of an arrangement of genotypes that are distinguished from each other by at least one mutation. Nonetheless, when the average genotypes of isolates from different infected plants are compared, the majority are almost identical. This suggests that in nature there is a strong selection pressure on infecting virus populations to maintain a state of equilibrium. We believe that the genetic structure (quasispecies) of viral populations influences their biological properties, such as host range, pathogenicity, and transmissibility, but few efforts have been made in plant virology to test this idea. It has been found that the number of different genotypes in an infecting virus population can be altered by the host environment, including host genotype, but this variability has not been correlated to any other characteristic of the host or biological property of the infecting viral population. Our working premise is that widespread planting of Rz1 resistant cultivars exerted selection pressure on BNYVV population structure which eventually led to emergence of resistance breaking isolates. The objective of this study was to identify and quantify the molecular changes that occur to an infecting BNYVV population when exposed to different host genotypes. Results of this study help explain how resistance breaking isolates evolve.