The arms race between beet necrotic yellow vein virus and host resistance in sugar beet.

Beet necrotic yellow vein virus (BNYVV) causes rhizomania disease in sugar beet (), which is controlled since more than two decades by cultivars harboring the resistance gene. The development of resistance-breaking strains has been favored by a high selection pressure on the soil-borne virus population. Resistance-breaking is associated with mutations at amino acid positions 67-70 (tetrad) in the RNA3 encoded pathogenicity factor P25 and the presence of an additional RNA component (RNA5). However, natural BNYVV populations are highly diverse making investigations on the resistance-breaking mechanism rather difficult. Therefore, we applied a reverse genetic system for BNYVV (A type) to study resistance-breaking by direct agroinoculation of sugar beet seedlings. The bioassay allowed a clear discrimination between susceptible and resistant plants already four weeks after infection, and resistance-breaking was independent of the sugar beet genotype. A comprehensive screen of natural tetrads for resistance-breaking revealed several new mutations allowing BNYVV to overcome . The supplementation of an additional RNA5 encoding the pathogenicity factor P26 allowed virus accumulation in the genotype independent of the P25 tetrad. This suggests the presence of two distinct resistance-breaking mechanisms allowing BNYVV to overcome . Finally, we showed that the resistance-breaking effect of the tetrad and the RNA5 is specific to and has no effect on the stability of the second resistance gene . Consequently, double resistant cultivars (+) should provide effective control of resistance-breaking strains. Our study highlights the flexibility of the viral genome allowing BNYVV to overcome host resistance, which underlines the need for a continuous search for alternative resistance genes.