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Rhizomania caused by Beet necrotic yellow vein virus (BNYVV) is a yield-limiting sugar beet disease that was observed to influence root resistance to freezing in storage. Thus, studies were conducted to gain a better understanding of the influence of BNYVV and freezing on sugar beet roots to improve pile management decisions. Roots from five commercial sugar beet cultivars (one susceptible and four resistant to BNYVV) were produced in fields under high and trace levels of rhizomania pressure and subjected to storage using five temperature regimes ranging from 0 to −4.4°C for 24 h. After cold treatment, eight-root samples were stored in a commercial indoor storage building (set point 1.1°C) for 50 days in 2014 and 57 days in 2015. Internal root temperature, frozen and discolored tissue, and moisture and sucrose loss were evaluated. The air temperature at 0, −1.1, and −2.2°C matched internal root temperature but internal root remained near −2.2°C when air temperature was dropped to −3.3 and −4.4°C. In a susceptible cultivar produced under high rhizomania pressure, the percentage of frozen tissue increased (P < 0.0001) from an average of 0 to 7% at 0, −1.1, and −2.2°C up to 16 to 63% at −3.3°C and 63 to 90% at −4.4°C, depending on year. Roots from the susceptible cultivar produced under low rhizomania pressure and those from the resistant cultivars from both fields only had elevated (P ≤ 0.05) frozen tissue at −4.4°C in 15 of 18 cultivar–year combinations. Frozen tissue was related to discolored tissue (r2 = 0.91), weight loss (r2 = 0.12 to 0.28), and sucrose reduction (r2 = 0.69 to 0.74). Consequently, BNYVV will not only lead to yield and sucrose loss in susceptible sugar beet cultivars but also to more frozen root tissue as temperatures drop below −2.2°C. Based on these observations, the air used to cool roots in nonfrozen sugar beet piles throughout the winter should not drop below −2.2°C to maximize sucrose retention.

Beet necrotic yellow vein virus (BNYVV) is the causal agent of rhizomania, a disease of global importance to the sugar beet industry. The most widely implemented resistance gene to rhizomania to date is Rz1, but resistance has been circumvented by resistance-breaking (RB) isolates worldwide. In an effort to gain greater understanding of the distribution of BNYVV and the nature of RB isolates in Minnesota and eastern North Dakota, sugar beet plants were grown in 594 soil samples obtained from production fields and subsequently were analyzed for the presence of BNYVV as well as coding variability in the viral P25 gene, the gene previously implicated in the RB pathotype. Baiting of virus from the soil with sugar beet varieties possessing no known resistance to rhizomania resulted in a disease incidence level of 10.6% in the region examined. Parallel baiting analysis of sugar beet genotypes possessing Rz1, the more recently introgressed Rz2, and with the combination of Rz1 + Rz2 resulted in a disease incidence level of 4.2, 1.0, and 0.8%, respectively. Virus sequences recovered from sugar beet bait plants possessing resistance genes Rz1 and/or Rz2 exhibited reduced genetic diversity in the P25 gene relative to those recovered from the susceptible genotype while confirming the hypervariable nature of the coding for amino acids (AAs) at position 67 and 68 in the P25 protein. In contrast to previous reports, we did not find an association between any one specific AA signature at these positions and the ability to circumvent Rz1-mediated resistance. The data document ongoing virulence development in BNYVV populations to previously resistant varieties and provide a baseline for the analysis of genetic change in the virus population that may accompany the implementation of new resistance genes to manage rhizomania.

Beet soilborne mosaic virus (BSBMV) is a rigid rod-shaped virus transmitted by Polymyxa betae. Particles were 19 nm wide and ranged from 50 to over 400 nm, but no consistent modal lengths could be determined. Nucleic acids extracted from virions were polyadenylated and typically separated into three or four discrete bands of variable size by agarose-formaldehyde gel electrophoresis. RNA 1 and 2, the largest of the RNAs, consistently averaged 6.7 and 4.6 kb, respectively. The sizes and number of smaller RNA species were variable. The molecular mass of the capsid protein of BSBMV was estimated to be 22.5 kDa. In Northern blots, probes specific to the 3′ end of individual beet necrotic yellow vein virus (BNYVV) RNAs 1–4 hybridized strongly with the corresponding BNYVV RNA species and weakly with BSBMV RNAs 1, 2, and 4. Probes specific to the 5′ end of BNYVV RNAs 1–4 hybridized with BNYVV but not with BSBMV. No cross-reaction between BNYVV and BSBMV was detected in Western blots. In greenhouse studies, root weights of BSBMV-infected plants were significantly lower than mock-inoculated controls but greater than root weights from plants infected with BNYVV. Results of serological, hybridization, and virulence experiments indicate that BSBMV is distinct from BNYVV. However, host range, capsid size, and the number, size, and polyadenylation of its RNAs indicate that BSBMV more closely resembles BNYVV than it does other members of the genus Furovirus.

A high degree of reciprocal cross-protection occurred in sugar beets between beet soilborne mosaic virus (BSBMV) and beet necrotic yellow vein virus (BNYVV) in greenhouse experiments. The incidence of cross-protection depended on the interval between inoculations with protecting and challenging virus; longer inoculation intervals enhanced the incidence of cross-protection. Cross-protection was most effective when the inoculation interval was between 5 and 10 days, a period during which virus accumulated to a maximum level in plants singly infected with BSBMV or BNYVV. Results obtained by enzyme-linked immunosorbent assay (ELISA) and Western blotting were consistent and indicated that cross-protection affected viral capsid protein accumulation. RNA of both protecting and challenging viruses was detected in doubly infected plants by using reverse transcription-polymerase chain reaction (RT-PCR), indicating that RNA of the challenge virus was present in protected plants, but capsid protein was undetected by serological tests. BSBMV is a closely related but serologically distinct virus that provides an excellent system for studies of cross-protection with BNYVV.

Beet necrotic yellow vein virus (BNYVV) causes rhizomania in beets. BNYVV is widespread in Europe and can be divided into an A and B group based on reverse transcription-polymerase chain reaction (RT-PCR) restriction fragment length polymorphism (RFLP) analysis (1). The vector of BNYVV, Polymyxa betae, is widespread in Denmark. However, surveys for BNYVV have regularly been carried out in Denmark since 1985, but it has not been detected until now. In the autumn of 2000, attention was drawn to a sugar beet field in the southeastern part of Denmark containing plants with unusually low sugar content. Typical BNYVV symptoms of bearded roots were observed on all plants sampled in the field. Root samples of 12 plants all tested positive for the presence of BNYVV by ELISA using antiserum from Adgen, Loewe, and Aschersleben, respectively. Immunosorbent electron microscopy with antiserum to BNYVV coat protein revealed decorated rod-shaped particles of lengths typical for BNYVV. Pulverized infected root tissue was used to mechanically inoculate Chenopodium quinoa and resulted in formation of few local chlorotic lesions. RNA was extracted from symptomatic C. quinoa and subjected to RT-PCR analysis using two primer sets specific for RNA 2 of BNYVV (1) and bands of the expected sizes were observed with both. The nucleotide sequence of a part of the PCR products corresponding to the N-terminus of the coat protein was determined and showed 99.5% identity to sequences derived from A group isolates (1). Finally, a bait-plant test was carried out, where sugar beet seeds were sown in 20 soil samples collected from different locations within the infested field. After 8 weeks of growth, all samples tested positive for the presence of BNYVV by ELISA, indicating that the entire field is infested and that viruliferous P. betae must have been present in several years. To our knowledge, this is the first record of BNYVV in Denmark. Reference: (1) M. Kruse et al. J. Gen. Virol. 75:1835, 1994.

The effects of cultivar mixtures and two irrigation frequency treatments were evaluated over two seasons for their impact on a complex of sugar beet root diseases in three fields infested with the fungal pathogens Aphanomyces cochliodes, Fusarium oxysporum f. sp. radicis-betae, Rhizoctonia solani, and the viral pathogen Beet necrotic yellow vein virus (BNYVV). Irrigations after emergence consisted of two or five (two 1994 studies) and three or six (1995 study) applications of water for dry and wet treatments, respectively. Cultivar treatments included MH9155, HH67, Ranger, Rhizosen, and four combinations of these same cultivars. Disease progress was monitored through destructive sampling of plants exhibiting foliar symptoms typical of root disease during the season. At harvest, data on root and sucrose yields, sucrose percentage, and a root disease index were collected. No significant irrigation × cultivar treatment interactions were observed. Few significant differences were observed between irrigation treatments involving measured yield components. Reduced irrigations however, resulted in significantly lower disease incidence in all three repeated experiments when cultivar treatments were combined. No added benefits were observed for increasing yield or decreasing root disease by planting mixed cultivars, compared to the same cultivars planted individually. Several regionally adapted cultivars performed as well or better than mixtures under the unusually high levels of disease pressure in test fields. When few alternative options are available, sugar beet growers may still benefit from reducing irrigations, and growing locally adapted cultivars in soils severely infested with root pathogens.

Rhizomania, caused by Beet necrotic yellow vein virus (BNYVV) and vectored by the soilborne fungus Polymyxa betae Keskin, is one of the most economically damaging diseases affecting sugar beet (Beta vulgaris L.). The virus likely originated in Europe and was first identified in California in 1983 (1). It has since spread among American sugar beet production regions in spite of vigorous sanitation efforts, quarantine, and disease monitoring (3). In the fall of 2002, mature sugar beet plants exhibiting typical rhizomania root symptoms, including proliferation of hairy roots, vascular discoloration, and some root constriction (2) were found in several fields scattered throughout central and eastern Michigan. Symptomatic beets were from numerous cultivars, all susceptible to rhizomania. Two to five sugar beet root samples were collected from each field and sent to the USDA-ARS in Salinas, CA for analysis. Hairy root tissue from symptomatic plants was used for mechanical inoculation of indicator plants. Mechanical inoculation produced necrotic lesions on Chenopodium quinoa and systemic infection of Beta vulgaris ssp. macrocarpa, both typical of BNYVV and identical to control inoculations with BNYVV. Symptomatic sugar beet roots were washed and tested using double antibody sandwich-enzyme linked immunosorbent assay (DAS-ELISA) for the presence of BNYVV using standard procedures and antiserum specific for BNYVV (3). Sugar beet roots were tested individually, and samples were considered positive when absorbance values were at least three times those of greenhouse-grown healthy sugar beet controls. Samples were tested from 16 fields, with 10 confirmed positive for BNYVV. Positive samples had mean absorbance values ranging from 0.341 to 1.631 (A405nm) after 30 min. The mean healthy control value was 0.097. Fields were considered positive if one beet tested positive for BNYVV, but in most cases, all beets tested from a field were uniformly positive or uniformly negative. In addition, soil-baiting experiments were conducted on seven of the fields. Sugar beet seedlings were grown in soil mixed with equal parts of sand for 6 weeks and were subsequently tested using DAS-ELISA for BNYVV. Results matched those of the root sampling. Fields testing positive for BNYVV were widely dispersed within a 100 square mile (160 km2) area including portions of Gratiot, Saginaw, Tuscola, and Sanilac counties in the central and eastern portions of the Lower Peninsula of Michigan. The confirmation of rhizomania in sugar beet from the Great Lakes Region marks the last major American sugar beet production region to be diagnosed with rhizomania disease, nearly 20 years after its discovery in California (1). In 2002, there were approximately 185,000 acres (approximately 75,00 ha) of sugar beet grown in the Great Lakes Region, (Michigan, Ohio, and southern Ontario, Canada). The wide geographic distribution of infested fields within the Michigan growing area suggests the entire region should monitor for symptoms, increase rotation to nonhost crops, and consider planting rhizomania resistant sugar beet cultivars to infested fields. References:(1) J. E. Duffus et al. Plant Dis. 68:251, 1984. (2) J. E. Duffus. Rhizomania. Pages 29–30 in: Compendium of Beet Diseases and Insects, E. D. Whitney and J. E. Duffus eds. The American Phytopathological Society, St. Paul, MN, 1986. (3) G. C. Wisler et al. Plant Dis. 83:864, 1999.

Rhizomania is an important virus disease of sugar beet and is caused by Beet necrotic yellow vein virus (BNYVV). During 2002-03, several sugar beet fields with cultivars partially resistant to BNYVV grown in the Imperial Valley of California were observed with severe rhizomania symptoms, suggesting that resistance conditioned by Rz1 had been compromised. Soil testing with sugar beet baiting plants followed by enzyme-linked immunosorbent assay (ELISA) was used to diagnose virus infection. Resistant varieties grown in BNYVV-infested soil from Salinas, CA, were ELISA-negative. In contrast, when grown in BNYVV-infested soil collected from the Imperial Valley, CA, all resistant varieties became infected and tested positive by ELISA. Based on host reaction, eight distinct BNYVV isolates have been identified from Imperial Valley soil (IV-BNYVV) by single local lesion isolation. Reverse transcription-polymerase chain reaction (RT-PCR) assays showed that the eight IV-BNYVV isolates did not contain RNA-5. Singlestrand conformation polymorphism banding patterns for the IV-BNYVV isolates were identical to A-type and different from P-type. Sequence alignments of PCR products from BNYVV RNA-1 near the 3′ end of IV-BNYVV isolates revealed that both IV-BNYVV and Salinas BNYVV isolates were similar to A-type and different from B-type. Our results suggest that the resistancebreaking BNYVV isolates from Imperial Valley likely evolved from existing A-type isolates.

During the 2001 growing season, a survey was conducted to determine the incidence of Beet necrotic yellow vein virus (BNYVV), Beet soilborne virus (BSBV), and Beet virus Q (BVQ) in Iran. A total of 2,816 random and 76 samples with rhizomania were collected from 131 fields in the main sugar beet cultivation areas of 13 provinces in Iran. All samples were tested using a tissue-blot immunoassay (TBIA) with commercial BNYVV (As-0799.1/CG6-F4), BSBV (As-0576.1), and BSBV/BVQ (As-0576.2) antisera provided by S. Winter (DSMZ, Braunschweig, Germany). For randomly collected samples, the highest incidence of virus infection was found for BNYVV (52.3%), followed by BSBV (9.5%) and BVQ (1.5%). Co-infection of BNYVV with BSBV or BVQ was 6.6% and 0.9%, respectively. Infection with both BSBV and BVQ was found in 16 (0.6%) samples. In addition, 0.4% (12) of the samples was infected with all three viruses. Our results indicated the presence of BVQ in samples from 10 fields located in Azarbayejan-e-gharbi, Esfahan, Fars, Kermanshah, Khorasan, Lorestan, and Semnan provinces of Iran, with or without rhizomania-like symptoms. The presence of viruses was confirmed using reverse transcription-polymerase chain reaction (RT-PCR) of RNA from 81, 19, and 14 root samples with positive reaction in TBIA to BNYVV, BSBV, and BVQ, respectively, with previously described primers (3,4). The primers specifically amplified fragments of 501 bp, 602 bp, 399 bp, and 291 bp of the BNYVV RNAs 1 and 4, BSBV RNA-2, and BVQ RNA-1, respectively. Our results indicated that the samples tested were also positive using RT-PCR. The putative vector for BNYVV, BSBV, and BVQ, Polymyxa betae, was also detected in 161 samples (from 127 fields) by amplification of a 170-bp fragment of the P. betae repetitive EcoRI-like fragments using previously described primers (4). RT-PCR products from 72 BNYVV-positive sugar beet root samples from 58 fields that also gave positive reactions in TBIA were analyzed using single-strand conformation polymorphism (SSCP) as previously described with extracts from root beards of the susceptible sugar beet cvs. OPUS and IC1 grown in the soils infested with BNYVV types A and B (provided by A. Meunier, Unite de Phytopathologie-UCL-AGRO-BAPA, Louvain-la-Neuve, Belgium) as positive controls (3). The patterns obtained with SSCP were uniform and showed widespread occurrence of BNYVV type A in almost all provinces surveyed. The fragments obtained for BNYVV RNAs 1 and 4 of an isolate from Qazvin (BNQ1) were sequenced (GenBank Accession Nos. AY703452 and AY703455) and compared with other sequences available in GenBank using Clustal W, which revealed 99.3 and 99.6% identity with the Japanese S (D84410) and Italian type A (AF197552) isolates, respectively. The economic importance of BVQ and its interactions with other sugar beet soilborne viruses remains a matter of debate. BNYVV and BSBV have been previously reported from Iran (1,2). To our knowledge, this is the first report of the natural occurrence of BVQ in sugar beets in Iran. References: (1) Sh. Farzadfar et al. Plant Dis. 86:187, 2002. (2) K. Izadpanah et al. Iran. J. Plant Pathol. 32:155, 1996. (3) R. Koenig et al. J. Gen. Virol. 76:2051, 1995. (4) A. Meunier et al. Appl. Environ. Microbiol. 69:2356, 2003.

Beet necrotic yellow vein virus (BNYVV), the casual agent of rhizomania disease, was identified in sugar beet plants from several fields in the Wielkopolska Region of Poland (1). In greenhouse studies, sugar beets were grown in the soil from one of these fields to bait soilborne viruses. Of 200 sugar beet plants, three developed symptoms of vein clearing, vein banding, and mosaic. Crude sap from symptomatic plants was used for mechanical inoculation of various plants species. In Chenopodium quinoa, C. amaranticolor, and Tetragonia expansa only local lesions were observed. Electron microscope examination of negatively stained leaf-dip preparations from symptomatic sugar beet plants showed a mixture of rod-shape particles from 70 to 400 nm long. Using double-antibody sandwich enzyme-linked immunosorbent assay tests, two symptomatic sugar beet plants gave positive reactions with antiserum against BNYVV (Bio-Rad, Hercules, CA) and a third plant gave a positive reaction with antisera against BNYVV and Beet soilborne virus (BSBV). Total RNA was extracted from roots and leaves of the symptomatic plants and used in a multiplex reverse transcription-polymerase chain reaction (mRT-PCR) assay. Specific primers were designed to amplify a fragment of the RNA1 for BSBV and RNA2 for BNYVV and Beet virus Q (BVQ) (2). Two mRT-PCR products amplified with the primers specific to BNYVV and BSBV were obtained and sequenced. A 274-nt amplicon sequence (GenBank Accession No. DQ012156) had 98% nucleotide sequence identity with the German BNYVV isolate F75 (GenBank Accession No. AF19754) and a 376-nt amplicon sequence (GenBank Accession No. AY999690) had 98% nucleotide and 98% amino acid sequence identity with the German BSBV isolate (GenBank Accession No. Z97873). The Polish BSBV isolate had 88% nucleotide and 62% amino acid sequence identity with BVQ, another pomovirus (GenBank Accession No. AJ 223596 formerly known as serotype Wierthe of BSBV (2). In 2005, mRT-PCR was used on samples collected from two fields of the Wielkopolska Region. Of 15 tested sugar beet plants, 12 gave positive reactions with primers specific for BSBV and nine with primers specific to BNYVV. To our knowledge, this is first report of BSBV in Poland. In Europe, BSBV was previously reported in England, the Netherlands, Belgium, Sweden, Germany, France, and Finland (2,3). References: (1) M. Jezewska and J. Piszczek. Phytopathol. Polonica, 21:165, 2001. (2) A. Maunier et al. Appl. Environ. Microbiol. 69:2356, 2003. (3) C. M. Rush and G. B. Heidel. Plant Dis. 79:868, 1995.

Beet necrotic yellow vein virus (BNYVV) is the type member of the genus Benyvirus and the causal agent of rhizomania disease of sugar beet. Since 1999, BNYVV is becoming one of the most important viruses of sugar beet in Poland. BNYVV is represented by three types, frequently A and B and rarely P, however, in Poland, type A only was recorded (2). In 2005, a survey was conducted to determine the incidence of types A and B of BNYVV in Poland. Thirty samples of sugar beet plants with rhizomania-like symptoms were collected from six fields in the western, southern, and northern areas of Poland. All samples were analyzed by double antibody sandwich-enzyme linked immunosorbent assay (DAS-ELISA) with commercial antiserum (Bio-Rad, Hercules, CA). Infection of BNYVV was found in 26 samples. The presence of the virus in these samples was confirmed by reverse transcription-polymerase chain reaction (RT-PCR). The total RNA extracted from sugar beet was tested with specific primers designed to amplify a fragment of the RNA2 for BNYVV (1). Multiplex (m) RT-PCR with two sets of primers, rhizo AF/rhizo AR and rhizo BF/rhizo BR (2), was used to distinguish A and B types of BNYVV. Two obtained mRT-PCR products were sequenced and compared with other sequences available in GenBank. A 121-nt amplicon sequence (GenBank Accession No. DQ 228872) had 100% nucleotide and amino acid sequence identity with all BNYVV type B sequences (e.g., Stourton-GenBank Accession No. AY682695) (2). A 171-nt amplicon sequence (GenBank Accession No. DQ228871) had 100% nucleotide and amino acid sequence identity with all BNYVV type A sequences (e.g., Ravenna-GenBank Accession No. AY 654282) (2). Type A was detected in 23 BNYVV-infected sugar beet plants from five fields located in western and southern Poland while type B was found in three samples from one field in northern Poland. To my knowledge, this is the first report of the natural occurrence of BNYVV type B in Poland. References: (1) A. Maunier et al. Appl. Environ. Microbiol. 69:2356, 2003. (2) C. Ratti et al. J. Virol. Methods 124:41, 2005.

In October of 2005, sugar beet (Beta vulgaris L.) plants exhibiting symptoms of rhizomania caused by Beet necrotic yellow vein virus (BNYVV) (3) were observed in a production field near Greeley, CO. The roots of seven plants exhibiting moderate to severe symptoms characteristic of this disease were tested using double-antibody sandwich enzyme-linked immunosorbent assay with anti-BNYVV antiserum from rabbits. Of these, only two roots exhibiting the mildest symptoms tested positive for BNYVV (all roots tested negative for the presence of the related Beet soilborne mosaic virus (BSBMV). ‘Hairy’ lateral roots characteristic of the disease were combined from the remaining five roots, ground in phosphate buffer, and the supernatant from the suspension was mechanically applied to leaves of Chenopodium quinoa in an effort to isolate an infectious agent. Five days postinoculation (dpi), yellow lesions with necrotic centers were visible on inoculated leaves, well in advance of those typically observed for BNYVV or BSBMV. Lesions exhibiting a similar rate of development on C. quinoa subsequently were induced from extracts of root vascular tissue prepared from four of seven additional beet roots tested from this location. Transfer of the infection from the C. quinoa lesions to 32 healthy C. quinoa and 10 sugar beet plants (hybrid ACH9369; American Crystal Sugar Co., Moorhead MN) resulted in 100% infection. Inoculated leaves of C. quinoa exhibited a high density of necrotic local lesions within 3 dpi, whereas inoculated leaves of sugar beet exhibited pinpoint, necrotic to diffuse, chlorotic local lesions evident by 5 dpi. Electron microscopic examination of fixed, ultra-thin sections of symptomatic C. quinoa leaf tissue revealed aggregates of virus-like particles of icosahedral symmetry within the cell cytoplasm. Following a virus minipreparation procedure, nucleic acid extracted from the partially purified virus was found to be single-stranded RNA by ribonuclease digestion and alone was infectious when inoculated to C. quinoa leaves. The apparently monopartite RNA genome was 3.5 kb long and a candidate for the single coat protein (CP) had a mass of ˜25 kDa. The sole reference set found in the literature for a virus naturally occurring on sugar beet with similar characteristics was that for Beet black scorch virus (BBSV), a virus recently accepted by the ICTV into the genus Necrovirus within the family Tombusviridae (2). Prior to this communication, BBSV has only been reported in China where it was first documented affecting sugar beet in the late 1980s (1). Using the published sequence of BBSV (Genbank Accession No. AY626780), DNA primers directed to the 3′ half of the BBSV genome were used in reverse transcription-polymerase chain reaction to produce an amplicon from the unknown virus. Sequencing the amplicon revealed 88.8% nucleotide sequence identity to the BBSV CP gene and 97% amino acid sequence identity to the predicted CP gene product. Combined, the nucleotide sequence and physical characteristics confirm the presence of BBSV in a U.S. sugarbeet field for the first time. To our knowledge, this is the first report of the occurrence of BBSV outside of China. References: (1) Y. Cao et al. Arch. Virol. 147:2431, 2002. (2) C. M. Fauquet et al. Eighth Report of the International Committee on the Taxonomy of Viruses. Academic Press, New York, 2005. (3) C. M. Rush. Ann. Rev. Phytopathol. 41:567, 2003.

During storage of sugar beet, respiration and rots consume sucrose and produce invert sugar. Diseases that occur in the field can affect the magnitude of these losses. This research examines the storage of roots with rhizomania (caused by Beet necrotic yellow vein virus) and the effectiveness of rhizomania-resistant hybrids in reducing postharvest losses. Roots of susceptible hybrids from sites with rhizomania had respiration rates 30 days after harvest (DAH) that ranged from 0.68 to 2.79 mg of CO2 kg–1 h–1 higher than roots of the resistant hybrids. This difference ranged from 2.60 to 13.88 mg of CO2 kg–1 h–1 120 DAH. Roots of resistant hybrids from sites with rhizomania had 18 kg more sucrose per ton than roots from susceptible hybrids 30 DAH, with this difference increasing to 55 kg Mg–1 120 DAH. The invert sugar concentration of susceptible hybrids from sites with rhizomania ranged from 8.38 to 287 g per 100 g of sucrose higher than that for resistant hybrids 120 DAH. In contrast, differences between susceptible and resistant hybrids in respiration rate, sucrose loss, and invert sugar concentration in the absence of rhizomania were relatively small. Storage losses due to rhizomania can be minimized by planting resistant hybrids and processing roots from fields with rhizomania soon after harvest.

In a survey of soilborne viruses infecting sugar beet in central Spain, Beet black scorch virus (BBSV) was detected in field grown sugar beets with symptoms of rhizomania disease. BBSV was found in all analyzed sugar beet producing regions from central Spain, as well as in bait plants grown in soils with a history of rhizomania from several Western European countries, thereby constituting the first report of BBSV in Europe. BBSV was transferred to Chenopodium quinoa, where it caused chlorotic local lesions from which virus particles were purified. The nucleotide sequence of the 3′-untranslated region of the genomic RNA was determined for 13 European isolates, and sequences were highly similar to those reported for Chinese and U.S. isolates. Sequence comparisons revealed three clusters of sequences, one including most European isolates, one including one European and two Chinese isolates, and the third including the U.S. isolate. BBSV was detected in a number of samples with rhizomania symptoms in which Beet necrotic yellow vein virus went undetected. However, its role in rhizomania disease in Europe, if any, remains to be established.

To reduce storage losses and improve resistance to rhizomania caused by Beet necrotic yellow vein virus (BNYVV), studies were initiated to establish a storage cultivar selection program. In 2006 and 2007, 30 or more commercial sugar beet (Beta vulgaris) cultivars were grown in soil naturally infested with BNYVV. At harvest, two root samples from each plot were collected and used to establish percent sugar. Additional samples were placed on top of an indoor pile (set point 1.7°C) and inside an outdoor pile in a randomized complete block design with four replications. After 142 and 159 days in indoor storage, sucrose reduction ranged from 13 to 90% in 2007 and 57 to 100% in 2008. Outdoor storage sucrose reduction ranged from 13 to 32% in 2007 and 28 to 60% in 2008. An average of 31 and 45% of the root surface was covered with fungal growth in 2007 and 2008, respectively. Cultivars that retained the most sucrose had resistance to BNYVV and the least fungal growth and weight loss. Indoor storage with BNYVV-infested roots allowed for the most consistent cultivar separation and will potentially lead to selection of cultivars for improved storability and rhizomania resistance.

Beet necrotic yellow vein virus (BNYVV) is an economically important pathogen of sugar beet (Beta vulgaris var. saccharifera) in several European, and Asian countries and in the United States (3). The virus is transmitted by the soil-inhabiting plasmodiophorid Polymyxa betae and causes the rhizomania disease of sugar beet. In November 2012, plants of B. vulgaris subsp. vulgaris cv. Boro (red table beet) exhibiting mainly severe characteristic root symptom of rhizomania were found in a commercial field located in the municipality of São José do Rio Pardo, State of São Paulo, Brazil. No characteristic virus-inducing foliar symptom was observed on diseased plants. The incidence of diseased plants was around 70% in the two visited crops. As the hairy root symptom is indicative of infection by BNYVV, the present study aimed to detect and identify this virus associated with the diseased plants. Preliminary leaf dip analysis by transmission electron microscopy revealed the presence of very few benyvirus-like particles. Total RNA was extracted from roots of three symptomatic plants and one asymptomatic plant according to Toth et al. (3). One-step reverse-transcription–polymerase chain reaction (RT-PCR) was performed as described by Morris et al. (2) with primers that amplify part of the coat protein gene at RNA2. The initial assumption that the hairy root symptom was associated with BNYVV infection was confirmed by the amplification of a fragment of ~500 bp from all three symptomatic samples. No amplicon was obtained from the asymptomatic control plant. Amplicons were directly sequenced, and the consensus nucleotide and deduced amino acid sequences showed 100% identity. The nucleotide sequence for one amplicon (Accession No. KM433683) was compared with other sequences deposited in GenBank. The nucleotide (468 nt) and deduced amino acid (156 aa) sequences shared 93 to 100 and 97 to 99% identity, respectively with the corresponding nucleotide and amino acid sequences for other isolates of type A of BNYVV. The virus was transmitted to three of 10 red table beet plants inoculated with contaminated soil, and infection was confirmed by nested RT-PCR, as described by Morris et al. (1), and nucleotide sequencing. This is the first report on the occurrence of BNYVV in Brazil, which certainly will affect the yield of red table beet in the producing region. Therefore, mapping of the occurrence of BNYVV in red table beet-producing areas in Brazil for containment of the spread of the virus is urgent. In the meantime, precautions should be taken to control the movement of contaminated soil and beet roots, carrots, or any vegetable grown on infested land that might introduce the virus to still virus-free regions. References: (1) J. Morris et al. J. Virol. Methods 95:163, 2001. (2) D. D. Sutic et al. Handbook of Plant Virus Diseases. CRC Press, Boca Raton, Florida, 1999. (3) I. K. Toth et al. Methods for the Detection and Quantification of Erwinia carotovora subsp. atroseptica (Pectobacterium carotovorum subsb. atrosepticum) on Potatoes: A Laboratory Manual. Scottish Crop Research Institute, Dundee, Scotland, 2002.

Root rots in sugar beet storage can lead to multimillion dollar losses because of reduced sucrose recovery. Thus, studies were conducted to establish additional fungicide treatments for sugar beet storage and a greater understanding of the fungi involved in the sugar beet storage rot complex in Idaho. A water control treatment and three fungicides (Mertect [product at 0.065 ml/kg of roots; 42.3% thiabendazole {vol/vol}], Propulse [product at 0.049 ml/kg of roots; 17.4% fluopyram and 17.4% prothioconazole {vol/vol}], and Stadium [product at 0.13 ml/kg of roots; 12.51% azoxystrobin, 12.51% fludioxonil, and 9.76% difenoconozole {vol/vol}]) were investigated for the ability to control fungal rots of sugar beet roots held up to 148 days in storage during the 2012 and 2013 storage seasons. At the end of September into October, roots were harvested weekly for 5 weeks from each of two sugar beet fields in Idaho, treated with the appropriate fungicide, and placed on top of a commercial indoor sugar beet storage pile until early February. Differences (P < 0.0001 to 0.0150) among fungicide treatments were evident. Propulse- and Stadium-treated roots had 84 to 100% less fungal growth versus the control roots, whereas fungal growth on Mertect-treated roots was not different from the control roots in 7 of 12 comparisons for roots harvested each of the first 3 weeks in both years of this study. The Propulse- and Stadium-treated roots also reduced (P < 0.0001 to 0.0146; based on weeks 1, 3, and 4 in 2012 and weeks 1, 3, 4, and 5 in 2013) sucrose loss by 14 to 46% versus the control roots, whereas roots treated with Mertect did not change sucrose loss compared with the control roots in 7 of 10 evaluations. The predominant fungi isolated from symptomatic roots were an Athelia-like sp., Botrytis cinerea, Penicillium spp., and Phoma betae. If Propulse and Stadium are labeled for use on sugar beet in storage, these fungicides should be considered for root rot control in commercial sugar beet storage and on roots held for vernalization for seed production of this biennial plant species.

Beet necrotic yellow vein virus (BNYVV) causes one of the most economically destructive diseases of sugar beet (Beta vulgaris), rhizomania, which may reduce sugar yield by 80%. This field investigation was conducted to evaluate the interactions between spinach genotypes and different BNYVV strains, and to determine whether BNYVV is transmitted through spinach seeds. Eight commercial spinach cultivars were planted in two BNYVV-infested fields and two control fields in Salinas, CA in 2009. Spinach plants in the BNYVV-infested fields showed disease symptoms of yellow-green or light-green vein clearing, mottling, or yellow-green chlorotic lesions on younger leaves as early as 28 days after planting (four- to six-true leaf stage). Leaves may also become stiff, more crinkled, and necrotic. There was an increase of lateral roots and leaf number but a decrease in leaf weight compared to healthy plants. Infected plants often became stunted, deformed, wilted, and dead. Symptomatic leaves and roots from plants with or without leaf symptoms in BNYVV-infested fields all tested positive for BNYVV by enzyme-linked immunosorbent assay. A more aggressive (resistance-breaking) strain of BNYVV led to higher disease incidence in spinach than in the wild type. BNYVV was not transmitted through spinach seeds. There were significant differences in disease development among cultivars, with disease incidence ranging from 8 to 44%, suggesting that genetic improvement of BNYVV resistance through spinach breeding should be feasible.

Rhizomania caused by Beet necrotic yellow vein virus (BNYVV) and storage losses are serious sugar beet production problems. To investigate the influence of BNYVV on storability, six sugar beet cultivars varying for resistance to BNYVV were grown in 2005 and 2006 in southern Idaho fields with and without BNYVV-infested soil. At harvest, samples from each cultivar were placed in an outdoor ventilated pile in Twin Falls, ID and were removed at 40-day intervals starting at the end of October. After 144 and 142 days in storage, sugar reduction across cultivars averaged 20 and 13% without and 68 and 21% with BNYVV for the 2005 and 2006 roots, respectively. In the December samplings, frozen root area was 1 and 2% without and 25 and 41% with BNYVV for the 2005 and 2006 roots, respectively. Root rot was always worse with stored roots from BYNVV-infested soil in December, January, and February samplings. Root weight loss was variable in 2005; however, in 2006, an increase in weight reduction always was associated with BNYVV-infested roots. In order to prevent losses in rhizomania-infested areas, cultivars should be selected for storability as well as rhizomania resistance.

Historically, Beet necrotic yellow vein virus (BNYVV), which causes the disease rhizomania of sugar beet, has caused major reductions in root yield and quality wherever it occurred. In the United States, the disease was first identified in California in 1984 (12), but it now occurs in every major sugar beet production region in the country. Fortunately, strong genetic tolerance to BNYVV, conferred by the Rz1 gene, was identified soon after rhizomania was discovered in the United States, and it has been incorporated into regionally adapted cultivars that allow profitable sugar beet production in areas infested with the pathogen. Plants possessing Rz1 are susceptible to infection by P. betae and BNYVV, but virus titers remain low, and typically, infected plants exhibit normal, asymptomatic growth. However, in the Imperial Valley of California in 2002, plants in a field planted to a rhizomaniatolerant cultivar began to express symptoms of rhizomania (47). Large strips of diseased plants occurred across the field, and it was soon verified that certain isolates of BNYVV from the California Imperial Valley (CIV-BNYVV) had overcome genetic resistance. In other regions of the United States, individual plants, or clusters of plants, in fields planted to rhizomaniatolerant cultivars have also become infected by BNYVV and developed diagnostic symptoms of severe rhizomania. Although patterns of disease development have varied between California fields and those in other production regions in the United States, the breakdown of genetic resistance has caused considerable concern among those involved in sugar beet production. The purpose of this article is to provide an update on rhizomania and the activities that are currently underway to manage this continuing threat to the U.S. sugar beet industry. A review on the detection and distribution of rhizomania and soilborne viruses associated with sugar beet production in the United States (61), and a second more in-depth review on BNYVV and its vector, Polymyxa betae (Keskin) (60), have been published.

Soils naturally infested with cultures of aviruliferous Polymyxa betae and viruliferous P. betae carrying two sugar beet benyviruses, Beet necrotic yellow vein virus (BNYVV) and Beet soilborne mosaic virus (BSBMV), alone and in combination, were compared with noninfested soil for their effects on seedling emergence, plant fresh weight, and virus content as measured by enzyme-linked immunosorbent assay (ELISA). Studies examined sugar beet with and without resistance to the disease rhizomania, caused by BNYVV. The Rz gene, conferring resistance to BNYVV, did not confer resistance to BSBMV. BSBMV ELISA values were significantly higher in single infections than in mixed infections with BNYVV, in both the rhizomania-resistant and -susceptible cultivars. In contrast, ELISA values of BNYVV were high (8 to 14 times the healthy mean) in single and mixed infections in the rhizomania-susceptible cultivar, but were low (approximately three times the healthy mean) in the rhizomania-resistant cultivar. Results indicate BNYVV may suppress BSBMV in mixed infections, even in rhizomania-resistant cultivars in which ELISA values for BNYVV are extremely low. Soils infested with P. betae, and with one or both viruses, showed significantly reduced fresh weight of seedlings, and aviruliferous P. betae significantly decreased sugar beet growth in assays.

Beet necrotic yellow vein virus (BNYVV) causes rhizomania of sugar beet (Beta vulgaris), which is characterized by stunting, leaf necrosis, constriction of the taproot, and extensive lateral- and feeder-root proliferation. Beet soilborne mosaic virus (BSBMV) causes similar but typically less severe symptoms than those of BNYVV. Both viruses are widely distributed in sugar beet-growing regions of the United States. Both viruses are vectored by the soilborne plasmodiophorid Polymyxa betae Keskin and are very similar in morphology and biology, sharing many characteristics in common. In 1999, soil samples were collected from sugar beet fields in Colorado, Minnesota, North Dakota, and Texas to determine the spatial association and covariation of the viruses in sugar beet fields. In 2000, additional samples were collected from fields in Minnesota and North Dakota. Over the 2-year period, soil samples were collected from 11 fields in various quadrat sizes. The viruses were assayed by growing sugar beet (cv. Beta 1395) in the soil samples and their incidence was determined using the double-antibody sandwich enzyme-linked immunosorbent assay. Both viruses were detected in samples from all fields but were in greater frequencies singly than in association. Association of the two viruses (where both viruses were detected in the same sample or bait plant) varied among fields, ranging from 1 to 42%. Geostatistical analysis revealed that both viruses, in large part, exhibited similar spatial patterns. In all but two fields, there was no spatial dependence among the sampling locations at sampled grid sizes. Their semivariances were constant at all separation distances in all directions indicating random spatial patterns. Overall, the spatial pattern of BNYVV appeared to be a little more structured than that of BSBMV. Even though both viruses are transmitted by the same vector and also exhibited similar distribution patterns, the incidence of one virus may not be estimated from that of the other due to lack of strong association and spatial dependence. However, similarity in spatial patterns of the two suggests that a similar sampling method can be employed for both viruses.

A field experiment was conducted to quantify the effects of different irrigation frequencies on sugar beet yield in pathogen-infested soils. Four irrigation regimes (every 2, 3, 4, and 5 weeks) and four inoculation treatments (beet necrotic yellow vein virus [BNYVV], beet soilborne mosaic virus [BSBMV], BNYVV+BSBMV, and a noninoculated control) were arranged in a split-plot design and replicated four times. Irrigation frequency and virus infection affected disease severity and yield. Sugar beets irrigated every 4 weeks had the lowest disease severity, and yield was not significantly different from the every 2 weeks frequency. Sucrose content was higher for beets in the 4-week irrigation treatment compared with the 2- and 3-week frequencies. Beets inoculated with BNYVV had higher disease severity and lower root yield than beets inoculated with BSBMV and BNYVV+BSBMV. A greenhouse experiment was conducted to evaluate the effect of water level on disease severity and water use in sugar beet. Four treatments (BNYVV, BSBMV, BNYVV+BSBMV, and a noninoculated control) and three water levels (pot capacity [PC], 75% PC, and 50% PC) were arranged in a split-plot design and replicated five times. Pots of each treatment were weighed every other day to determine evapotranspiration. Evaporation was determined from unplanted pots, and plant transpiration was calculated by the difference. Beets irrigated at 75% pot capacity showed minimal disease incidence and a root weight comparable to the fully irrigated healthy control. Plants in the BNYVV treatment had a significantly higher disease severity than beets infected by BSBMV or BNYVV+BSBMV. Root weights and plant water use were significantly affected by virus infection. Beets in the BNYVV+BSBMV treatment had a significantly higher root dry weight and water use than beets in the BNYVV treatment, suggesting that BSBMV reduced the impact of disease caused by BNYVV.

Levels of beet necrotic yellow vein virus (BNYVV), as measured by triple-antibody sandwich-enzyme-linked immunosorbent assay (TAS-ELISA), were compared with biological evaluations in representative commercial and experimental sugar beet cultivars developed for production in the United States and ranging in their reactions to rhizomania from uniformly susceptible to highly resistant. TAS-ELISA was specific for BNYVV and did not react with related soilborne sugar beet viruses. Differences in absorbance (A405nm) values measured in eight cultivars closely correlated with the dosage and frequency of the Rz allele, which conditions resistance to BNYVV. A diploid (Rzrz) hybrid had a significantly lower absorbance value (less virus) than a similar triploid (Rzrzrz) hybrid. Cultivars that segregated (Rzrz:rzrz) had higher absorbance values than uniformly resistant (Rzrz) hybrids, as was expected. For all cultivars, absorbance values decreased as the season progressed. Absorbance value was significantly positively correlated with rhizomania disease index score and negatively correlated with individual root weight, plot root weight, and sugar yield. This information should be useful in resistance-breeding and -evaluation programs and in the sugar industry when considering cultivar choice, inoculum production, and future crop rotations.

Sugar beet (Beta vulgaris var. saccharifera L.) is the main crop used for the production of sugar in Croatia. Beet yellows virus (BYV), type member of the genus Closterovirus, is characterized by flexuous, filamentous particles which are transmitted by several aphid species in a semipersistent manner (Agranovsky and Lesemann 2000). This widely spread virus is reported from most of the sugar beet-growing areas of the world, including Europe. In the geographic region that was once the former Yugoslavia, the presence of BYV was suspected based on field symptoms reported from Serbia (Nikolić 1951) and Croatia (Panjan 1951). During the 2013 and 2014 growing season, the presence of sugar beet plants with symptoms of yellowing was sporadically observed in commercial fields located in eastern Croatia (i.e., Tovarnik, Bošnjaci, and Virovitica). In late July 2014, a significant number of sugar beet plants, located mainly on the field edges, with the aforementioned symptoms were noticed in experimental fields of various sugar beet cultivars located at the University of Zagreb, Faculty of Agriculture. In total, 102 plants collected from commercial fields and 12 plants from the university experimental fields with cvs. Torda and Libero were selected and screened using ELISA for the presence of Beet necrotic yellow vein virus (BNYVV), Beet mosaic virus (BtMV), Beet mild yellowing virus (BMYV), Beet western yellows virus (BWYV), and BYV. To conduct the diagnostic assays, commercial ELISA kits from Loewe Biochemica GmbH (BNYVV, BtMV, and BYV) and Sediag (BMYV and BWYV) were used. BYV was confirmed in five plants from commercial fields and in all the plants from Zagreb. Due to the presence of single infections in plants from Zagreb, and in order to determine the detrimental effects of BYV, all plants from the study field control plots (104 of Torda and 103 of Libero) were tested by ELISA. Tests revealed the presence of BYV in 18 (17.3%) plants of Torda and in 34 (33%) plants of Libero. BYV infections averaged a 9 to 10% reduction of pure root yield and sugar content in both cultivars compared with BYV-free plants. One ELISA-positive plant per cultivar was chosen for the extraction of total RNA using the QIAGEN RNeasy plant mini kit according to manufacturer’s instructions. In both plants, the presence of BYV was confirmed by RT-PCR using four set of diagnostic primers (Kundu and Ryšánek 2004). PCR products from both samples, named BYV- CRO-T from Torda and BYV-CRO-L from Libero, were purified and sequenced in both directions (Genbank Accession Nos. KP704263 to KP704268). Nucleotide sequence alignment of the DNA fragments for both Croatian isolates, including the C-terminal part of L-Pro and N-terminal part of MET and HSP70, showed 99.2, 99.7 and 100% similarity, respectively. Nucleotide comparisons of Croatian isolates with Californian (Genbank Accession No. AF056575) showed a 97% similarity for L-Pro and HSP70 and a 99% for MET. To our knowledge, this is the first report of Beet yellows virus in Croatia and its detrimental effect on actual sugar beet cultivars grown under Croatian environmental conditions.

The objective of this work was to determine whether Beet virus Q (BVQ), a member of the genus Pomovirus, is present in Poland. BVQ, like Beet necrotic yellow vein virus (BNYVV), is transmitted by Polymyxa betae Keskin. Earlier, BVQ was described as the Wierthe serotype of Beet soilborne virus (BSBV). Now, on the basis of its genomic properties (2), BVQ is recognized as a distinct virus species. BVQ is often found in fields where BSBV and BNYVV are present (4). During the fall of 2005, five plants of a cultivar susceptible to rhizomania (cv. Alyssa) and five resistant to rhizomania (cv. Henrietta) were collected from a field in the Wielkopolska Region of Poland, where BSBV and BNYVV had been previously identified, and tested for BVQ (1). All samples were analyzed by a double antibody sandwich-enzyme linked immunosorbent assay (DAS-ELISA) with antiserum against BNYVV (Bio-Rad, Hercules, CA). Rhizomania was identified only in sugar beet samples of the susceptible variety. The same samples were then tested using a triple antibody sandwich (TAS)-ELISA with commercial antisera against BSBV/BVQ (As-0576.2) and BSBV (As-0576.1) (DSMZ, Braunschweig, Germany). Nine sugar beet plants gave positive reactions with antiserum against BSBV/BVQ and negative reactions with antiserum specific to BSBV. Total RNA extracted from roots of 10 beet samples was then tested using a multiplex reverse transcription-polymerase chain reaction (mRT-PCR) and specific primers designed to amplify a fragment of the RNA2 for BNYVV and BVQ (3). The primers specifically amplified fragments of 545 bp and 291 bp of the BNYVV and BVQ, respectively. BNYVV was detected in all five samples from susceptible sugar beet plants. The presence of BVQ was confirmed in nine of the sugar beer plants, and the RT-PCR products were sequenced. Sequence analysis of the 206-nt amplicon sequence of the Polish isolate of BVQ (GenBank Accession No. DQ309444) indicated 97% nucleotide and 94% amino acid sequence identity with the previously published sequence of BVQ (GenBank Accession No. AJ223596) (2). To my knowledge, this is the first report of the natural occurrence of BVQ on sugar beet in Poland. In Europe, it has been previously reported in Belgium, Bulgaria, France, Germany, Hungary, Italy, the Netherlands, Spain, and Sweden (3,4). References: (1) N. Borodynko et al. Plant Dis. 90:112, 2006. (2) R. Koenig et al. J. Gen. Virol. 79:2027, 1998. (3) A. Meunier et al. Appl. Environ. Microbiol. 69:2356, 2003. (4) C. Rubies Autonell et al. Plant Dis. 90:110, 2006.

Rhizomania, caused by Beet necrotic yellow vein virus (BNYVV) and vectored by the soilborne fungus, Polymyxa betae Keskin, is one of the most economically damaging diseases affecting sugar beet (Beta vulgaris L.) worldwide and has been found in most sugar beet-growing areas of the United States (2). During harvest in October 2000, sugar beet plants exhibiting typical symptoms of rhizomania (1) were found in a field near Paterson, WA. Sugar beet had been planted in the field in 1999 and 2000, but prior to this, the field had not been planted with sugar beet for approximately 20 years. Symptomatic roots from the field exhibited stunting, vascular discoloration, and proliferation of lateral rootlets. Leaves of affected plants were chlorotic. Four soil samples were taken from symptomatic areas of the field and diluted with an equal amount of sterile sand. Seeds of rhizomania-susceptible sugar beet cv. Beta 8422 were planted in the soil and sand mix and maintained in a controlled environment at 24°C and 12 h of daylight at one location and in the greenhouse at another. After 8 weeks, enzyme-linked immunosorbent assay (ELISA) was performed on roots of plants grown at each location. Triple-antibody sandwich (TAS) ELISA (Agdia, Inc., Elkhart, IN) was conducted at the University of Idaho, Twin Falls, ID and double-antibody sandwich (DAS) ELISA was performed at USDA-ARS, Salinas, CA, with antiserum specific for BNYVV (2). Two of four samples were positive for BNYVV in the ELISA tests at both locations based on absorbance values at least three times those of healthy controls. TAS-ELISA tests were conducted on roots collected in July 2001 from a field in Washington, 12.9 km from the first field, as well as from a field across the Columbia River near Boardman, OR. Samples from both fields tested positive for BNYVV. All three fields are within 24 km of one another. Four additional fields have subsequently been confirmed to be infected with BNYVV in this region, based on symptomology and ELISA. There are approximately 3,240 ha of sugar beet grown in the region, and growers have been advised as a result of this confirmation to plant resistant cultivars and increase the sugar beet rotation interval with nonhost crops to a minimum of 4 years. References: (1) J. E. Duffus. Rhizomania. Pages 29–30 in: Compendium of Beet Diseases and Insects. E. D. Whitney and J. E. Duffus, eds. The American Phytopathological Society, St. Paul, MN, 1986. (2) G. C. Wisler et al. Plant Dis. 83:864, 1999.

Beet necrotic yellow vein virus (BNYVV), the causal agent of rhizomania disease on sugar beet, has been reported in Belgium for more than 16 years. Other soilborne viruses belonging to the genus Pomovirus, such as Beet soilborne virus (BSBV) (3) and Beet virus Q (BVQ) (1), are suspected pathogens of sugar beets grown in Belgium. During the 2000 growing season, more than 20 fields showing rhizomania-like and yellowing symptoms on sugar beet leaves were investigated for the presence of BVQ, BNYVV, and BSBV. All samples were checked by enzyme-linked immunosorbent assay (ELISA) using commercial BNYVV (Sanofi Diagnostics Pasteur, Marnes-La-Coquette, France) and BSBV/BVQ (DSMZ, Braunschweig, Germany - AS-0576 polyclonal, AS-0576/2 MAb) antisera. RNA was extracted from sugar beet rootlets using an RNeasy extraction kit (Qiagen, Hilden, Germany), before performing a reverse transcription-polymerase chain reaction (RT-PCR) using primers (5′-GCTGGAGTATATCACCGATGAC-3′ and 5′-AAAATC TCGGATAGCATCCAAC-3′) designed to specifically amplify a 510-bp region of BVQ RNA-1. The presence of BSBV and BNYVV was also checked by RT-PCR using previously described primers (1,2). The BVQ-derived PCR product was sequenced and proved to be more than 99% identical to the Wierthe BVQ isolate nucleotide sequence. Soil transmission of BVQ was demonstrated through a bioassay using soil dilutions with quartz and sugar beet cv. Cadyx as bait. After 6 weeks, BVQ was detected by RT-PCR in bait plants. The putative vector, Polymyxa betae, was identified by lactophenol-cotton blue staining of the roots followed by microscopic examination. BVQ produces irregularly shaped local lesions that appear ≈5 days after mechanical inoculation and tend to spread along veins. BVQ was detected in six fields located in the Polders Region and Brabant Province of Belgium. BVQ was always found in sugar beet samples coinfected with BNYVV and BSBV. The economic significance of BVQ and its interaction with other viruses is not known. References: (1) R. Koenig et al. J. Gen. Virol. 79:2027, 1998. (2) M. Saito et al. Arch. Virol. 141:2163, 1996. (3) M. Verhoyen and M. Van den Bossche. Parasitica. 44:71, 1987.

Field studies were conducted in 1991 and 1993 to evaluate the effectiveness of Tolene II fumigation and rhizomania-tolerant cultivars to control a complex of soilborne pathogens (Rhizoctonia solani, Aphanomyces cochlioides, Fusarium oxysporum f. sp. betae, and beet necrotic yellow vein virus). Fifteen cultivars (13 rhizoimania-tolerant and two rhizomania-susceptible) were included in a randomized complete block split-plot design with six replications in which main plots were fumigated or nonfumigated and cultivars were subplots

The Texas sugar beet-growing area was surveyed to determine the incidence of beet necrotic yellow vein virus (BNYVV), beet distortion mosaic virus (BDMV), and an unnamed soilborne sugar beet virus designated as Texas 7 (Tx7). In late 1990, 302 soil samples were collected from seven Texas counties and one New Mexico county from fields scheduled for 1991 production. Sugar beet seed was planted in the soil samples, and root tissue was later harvested and tested by ELISA. Of 174 soil samples screened for BNYVV, 19 were positive. Of 128 samples tested for BNYVV and Tx7, 12 were positive for Tx7, three were positive for BNYVV, and 23 were positive for both BNYVV and Tx7 [...]