The Beet necrotic yellow vein virus (BNYVV) causes rhizomania disease in sugar beet leading to massive yield losses. All sugar beet cultivars carry the Rz1 resistance gene, but there are several reports
describing the occurrence of Rz1 resistance breaking strains. The high selection pressure leads to several mutations in the pathogenicity factor P25 at amino acid positions 67-70 (tetrad). An additional
RNA component from the P-type (RNA5) has been also associated with Rz1 resistance breaking.Consequently, field populations from BNYVV must be continuously monitered for their ability to
overcome Rz1 resistance. Therefore, we characterized field populations from BNYVV for their Rz1 resistance-breaking properties using bait plant tests and molecular tools. A reverse genetic system was
applied to confirm the resistance breaking properties of P25 mutations. We could identify several populations able to overcome Rz1 resistance. Sequencing of P25 revealed the presence of multiple
tetrad variants. We could observe unexpected combinations of virus type and tetrad variants suggesting genetic reassortments. Several populations possessed an additional RNA5. Using a reverse
genetic system for BNYVV, we showed that multiple tetrad variants are able to mediate resistance breaking in sugar beet. The ability of RNA5 to mediate resistance-breaking independent of P25 could
be demonstrated. The results highlight the ongoing adaption of BNYVV populations to Rz1 resistance in sugar beet. BNYVV seems to have developed different strategies to cope with Rz1 resistance either
by mutation of P25 or the presence of additional RNA components (RNA5).