LUTEOVIRUS (LUTEOVIRIDAE)

Taxonomy

Luteoviridae are spherical, phloem-limited, aphid transmitted plant viruses, containing a positive-sense genomic RNA. In 1998, the International Committee on the Taxonomy of Viruses (ICTV) raised the luteovirus group to the level of family. The new Luteoviridae family now contains three genera: the genus Luteovirus (formerly known as luteovirus subgroup I), the genus Polerovirus (formerly known as luteovirus subgroup II), and the genus Enamovirus which consists solely of pea enation mosaic virus-1. This entry refers only to the luteoviruses and poleroviruses. Another entry discusses the genus Enamovirus. Members of the Luteovirus and Polerovirus genera have distinctly different genome organizations, cytopathological effects and serological properties. The differences and similarities between the two genera will become evident throughout this entry.

A list of Luteoviridae and their vectors is shown in Table 1 . Barley yellow dwarf virus (BYDV), beet western yellows virus (BWYV) and potato leafroll virus (PLRV) are the best characterized, so most discussion will focus on these. Several viruses on this list may be strains of a single virus, because Luteoviridae (1) are difficult to identify by symptomatology, (2) are difficult to purify, (3) show varying degrees of serological crossreactivity, and (4) vary in host range, depending on the isolate. For example, soybean dwarf (SBDV) and subterranean clover red leaf (SCRLV) viruses are so closely related serologically that they may be strains of the same virus. However, a Mississippi isolate of SCRLV is unable to infect soybeans.

Table 1.

Luteoviridae classification

Virus	Abbreviation	Vectora
Luteovirus genus
Barley yellow dwarf-PAV	BYDV-PAV	Rhopalosiphum padi, Sitobion avenae
Barley yellow dwarf-MAV (rice giallume)	BYDV-MAV	S. avenae
Probable Luteovirus
Soybean dwarfb (strawberry mild yellow edge)	SBDV	Aulacorthum solani
Subterranean clover redleaf	SCRLV	A. solani
Polerovirus genus
Cereal yellow dwarf-RPV (formerly BYDV-RPV)	CYDV-RPV	R. padi
Beet western yellows (malva yellows) (turnip mild yellows)	BWYV	Myzus persicae
Beet mild yellowing	BMYV	M. persicae
Cucurbit aphid-borne yellows	CABYV	M. persicae, Aphis gossypii
Potato leaf roll (Solanum yellows) (tomato yellow top)	PLRV	M. persicae
Probable polerovirus
Barley yellow dwarf-RMV	BYDV-RMV	Rhopalosiphum maidis
Carrot red leaf	CRLV	Cavariella aegopodii
Cereal yellow dwarf virus – GPV (formerly BYDV-GPV)	CYDV-GPV	Schizaphis graminum
Groundnut rosette assistor	GRAV	Aphis craccivora
Genus uncertain (Luteovirus or Polerovirus)
Barley yellow dwarf-SGV	BYDV-SGV	Schizaphis graminum
Bean leaf roll = pea leaf roll (pea leaf roll) (Michigan alfalfa) (legume yellows)	BLRV	M. persicae
Chickpea stunt associated	CpSaV	M. persicaec
Sweet potato leaf speckling	SPLSV	Macrosiphum euphorbiae
Tobacco necrotic dwarf	TNDV	M. persicae
Solanum yellows	SYV	M. persicae
Indonesian soybean dwarf	ISDV	Aphis glycines
Enamovirus genus
Pea enation mosaic virus-1	PEMV-1	M. persicae

Synonyms are in parentheses. Probable members of genera have been assigned by the author, not the ICTV.

Modified from D'Arcy et al (1999).

^aFor each virus, the best characterized vector is shown. In some cases, several aphid species serve as vectors.

^bHas been proposed to be in a third subgroup owing to structural genes that are most closely related to those of poleroviruses, and absence of ORF 6.

^cLess than 10% transmission efficiency.

In contrast to potentially synonymous viruses, BYDV has been split into two viruses. Originally, five serotypes were defined by the different aphid vectors that transmit them (Table 1). Furthermore, isolates of a serotype can vary greatly in symptom severity in a given host, and one isolate can cause widely varying symptoms in different hosts. Because of major differences in genome organization and cytopathology, BYDV serotypes have been divided among luteoviruses and poleroviruses. BYDV-PAV and BYDV-MAV are closely related strains of BYDV, the only official luteovirus; while the former BYDV-RPV is now called cereal yellow dwarf virus-RPV and assigned to the Polerovirus genus.

Geographic Distribution

BWYV, PLRV, BYDV and carrot red leaf virus (CRLV) have worldwide distributions. BYDV or cereal yellow dwarf virus (CYDV) have been reported virtually wherever wheat, barley or oats are grown. Tobacco necrotic dwarf virus (TNDV) and SBDV are limited to Japan. Isolates of SCRLV, which have been considered synonymous to SBDV, occur in Australia and the southern USA, but the American isolate does not infect soybean. Groundnut rosette assistor virus (GRAV) occurs only in Africa.

Host Range

Most luteoviruses have limited host ranges. BWYV stands out with its very wide range of dicotyledonous hosts, although very few isolates actually infect beets. In contrast, the more common beet-infecting luteovirus is beet mild yellowing virus (BMYV). Because PLRV, which is limited to the Solanaceae, and BWYV both have the same vector, host range is not determined merely by the host range of the vector. BYDV and CYDV infect most if not all members of the Graminae. CRLV is the only luteovirus known to infect the Umbelliferae.

Virus Structure and Composition

Luteoviridae particles are icosahedral, T = 3, with a diameter of 24–30 nm. They contain 180 subunits of a 22 kDa coat protein. A small, undetermined number of coat protein subunits contain an additional 50–53 kDa polypeptide fused to the C-terminus, produced by translational readthrough of the coat protein gene stop codon. The virion is 28% RNA by weight. It contains a 5.5–6 kb genomic RNA. A genome-linked protein (VPg) with reported molecular weights of either 7 kDa (PLRV) or 17 kDa (CYDV) is attached covalently to the 5′ end of the genomic RNA of poleroviruses. BYDV RNA lacks a VPg or any other known modification. The 3′ end of the genomic RNA contains neither a poly (A) tail nor a tRNA-like structure.

Replication

Genome organization

Luteoviridae have a positive-sense RNA genome encoding 5–6 open reading frames (ORFs) (Fig. 1 ). Different genome organization is a major distinction between the Luteovirus and Polerovirus genera (Fig. 1). Poleroviruses have a gene (ORF 0) at the 5′ end of the genome that encodes a 28–29 kDa protein (P0) which is absent in luteoviruses. Luteoviruses contain an ORF encoding a 4–7 kDa protein (P6) that is absent in poleroviruses. SBDV, while resembling luteoviruses in untranslated sequences, RNA-dependent RNA polymerase (RDRP), and genome organization, lacks ORF 6 and is more homologous to poleroviruses in the structural genes.

Figure 1.

Genome organizations of Luteoviridae: (A) Luteovirus; (B) Polerovirus. Molecular weights of proteins encoded by each ORF are indicated in kilodaltons (K). Unshaded, no homology to known proteins; checkered, highest homology to diantho- and carmoviruses; light shading, highest homology to sobemoviruses; dark shading, highest homology to other Luteoviridae. Functions of proteins are indicated where known: PRO, putative protease; VPg, genome-linked protein; POL, RNA-dependent RNA polymerase; CP, coat protein; AT, aphid transmission; MP, probable movement protein. Positions of subgenomic RNAs (thinner lines) are indicated below genomic RNA (bold line).

Protein functions

The functions of P0 and P6 are unknown. The products of ORFs 0, 3, 4, 5 and 6 are unnecessary for RNA replication in protoplasts, but some of them can increase the accumulation of viral RNA. The product of ORF 2 is expressed only as a C-terminal fusion with ORF 1 (P1–2). ORF 2 encodes the RDRP component of the replicase. P1 of poleroviruses contains the catalytic triad of amino acids conserved among cysteine proteases. Downstream of this region, but upstream of the frameshift site, P1 also contains the VPg amino acid sequence. Thus, the VPg is made available presumably by proteolytic cleavage of P1 and/or P1–2. P3 is the major coat protein (CP). A minor portion of the coat proteins produced in infection consists of a fusion of P3 and P5 made by translational readthrough of the ORF 3 stop codon. P4 is necessary for systemic infection of plants by BYDV, but not by BWYV. Evidence supports a role in cell-to-cell movement for P4 of PLRV: it is associated with plasmodesmata and fragments of this phosphorylatable protein have noncovalent, nonspecific single-stranded nucleic acid binding properties. The P3–5 translational readthrough product is often found cleaved about midway in the P5 domain. The N-terminal portion of P5 is necessary and sufficient (when fused to coat protein on virions) for aphid transmission. The C-terminal portion of P5 may be involved in virus movement within the plant, at least for BWYV.

Transcription

Although only the genomic RNA is encapsidated, subgenomic (sg) RNAs are produced by RNA-templated transcription in the infected cell. ORFs 3, 4 and 5 are translated from subgenomic mRNA 1 (sgRNA1) (Fig. 1). In BYDV, smaller sgRNAs 2 and 3 are also produced. These RNAs may serve a regulatory function. sgRNA2 is predicted to be an efficient message for ORF 6 and functions as such in vitro. In cells infected with PLRV or cucurbit aphid-borne yellows virus (CABYV), sgRNA2 may also be a message for small ORFs. Presence of the ST9-associated RNA increases the abundance of sgRNA2 in BWYV-infected cells (below).

All sgRNAs are 3′-coterminal with the genomic RNA and are present in abundance that is roughly inversely proportional to their size. The 5′ termini of sgRNAs and genomic RNA begin with common sequences. In poleroviruses, sobemoviruses and dianthoviruses this sequence is ACAAAA. In luteoviruses the consensus is AGUGAAGA. These sequences or their complements are likely involved in replicase promoters. The ACAAA motif is unusually abundant throughout the genomes of all luteo- viruses.

Translation

Luteoviridae employ a plethora of rare translational events to control gene expression. BYDV RNA lacks a 5′ cap (m⁷GpppN). A sequence located, surprisingly, in the 3′ end of the genome facilitates efficient cap-independent translation. The polymerase gene (ORF 2) is expressed only via a ‘−1’ ribosomal frameshift that occurs during translation of ORF 1 in the region where the two ORFs overlap. At a low frequency, elongating ribosomes slip back one nucleotide, moving from ORF 1 to ORF 2, resulting in a low abundance fusion protein comprising these two ORFs. Ribosomal frameshifting facilitates synthesis of low levels of polymerase, an enzyme needed in only small quantities, and high levels of its N-terminal region, P1, whose function by itself is unknown. Some of the cis-acting signals that mediate this event – a shifty heptanucleotide followed by a highly structured sequence – are similar to those which induce −1 frameshifting in translation of the polymerases of corona viruses and retroviruses. However, in the case of BYDV, sequences located several kilobases downstream in the 3′ untranslated region of the genome, are also necessary for frameshifting. This differs dramatically from other known frameshift signals.

Translation initiates at the start codons of ORFs 3 and 4 by leaky scanning on sgRNA001. This mechanism may also apply to translation of the overlapping ORFs 0 and 1 from genomic RNA of poleroviruses. ORF 5 is expressed by occasional in-frame readthrough of the coat protein stop codon, giving rise to the P3–5 fusion protein. A nucleotide tract harboring 8–16 multimeric CCXXXX repeats just downstream of the ORF 3 amber stop codon, as well as a sequence about 750 nt downstream, are necessary for readthrough.

Luteoviridae-associated RNAs

A 322 nucleotide satellite RNA (satCYDV RNA, formerly satRPV or sBYDV RNA) was discovered in an Australian isolate of CYDV-RPV. satCYDV RNA replicates by a symmetrical rolling circle mechanism. Hammerhead self-cleavage structures exist in the plus (encapsidated) and minus strands of the RNA. satCYDV RNA reduces CYDV-RPV helper virus levels and ameliorates disease symptoms in infected oat plants. It is not supported by BYDV, but its replication is supported by BWYV in dicotyledonous hosts. Thus, a component provided by poleroviruses is necessary for replication, and the host range of the helper virus may define the satellite's host range.

Additional RNAs have been found associated with a severe isolate of BWYV called ST9 and with CRLV. These 3 kb RNAs encode RDRP sequences that are more similar to luteovirus RDRPs than those of poleroviruses, to which BWYV and CRLV belong. They can replicate independently in protoplasts, but depend on their helper viruses for encapsidation and efficient spread in plants. Both of the associated RNAs enhance accumulation of their helper viruses. This typifies a phenomenon in Luteoviridae in which RNAs harboring luteovirus-like and polerovirus-like RDRP genes, enhance each others' accumulation. These cross-enhancing interactions range from mixed infections of BYDV and CYDV viruses, to complete interdependence of two such RNAs in pea enation mosaic virus (PEMV). PEMV, the sole member of the Enamovirus genus, consists of two particles. Each PEMV RNA can replicate autonomously in plant cells, but both are required to form a viable agent in the field. PEMV1 has a polerovirus-like RDRP while the PEMV2 RDRP resembles those of luteoviruses and umbraviruses.

Evolution

As discussed above, the 5′ halves of the genomes of the Luteoviridae have two separate origins (Fig. 1). The RDRP genes of luteoviruses are most similar to the RDRP genes of the umbra- carmo-, tombus- and dianthoviruses. The RDRP genes of poleroviruses are more closely related to those of the sobemoviruses than to those of luteoviruses. In contrast, the genes in the 3′ halves of the genomes of all Luteoviridae, are more similar to each other than to genes of any other virus family or genus. Hence, these must be the genes that confer the biological properties that make the Luteoviridae a distinct family. Because of the divergent origins of luteoviral genomes it is obvious that Luteoviridae do not descend from a common ancestor. Instead, horizontal exchanges of genes must have occurred to generate the two main genera.

Additional divergence between halves of the genome exists within genera. BWYV and BMYV have around 90% amino acid sequence identity in the structural genes, but less in the polymerase genes and only 25% and 34% identity in ORFs 0 and 1, respectively. Yet BMYV and CABYV are 42% and 49% identical in these ORFs but only 63% identical in the CP and 39% identical in the P5 domain. Similarly, Mexican and Californian isolates of CYDV-RPV are 90% identical to the New York CYDV-RPV isolate in structural genes, but show no homology in ORF 0 detectable by northern blot or polymerase chain reaction (PCR).

The sharpest point of divergence in sequence homology both within and between subgroups is at or near the region that separates the RDRP and structural genes. This is also the site of the promoter for sgRNA001. Thus it is possible that recombination occurs by replicase strand-switching at sgRNA promoters.

Comparison of luteovirus sequences with other viruses has revealed striking evolutionary relationships. The genome organization of PEMV1 RNA is similar to that of poleroviruses, except that it lacks ORF 4, and ORF 5 is only 33 kDa. All the ORFs of RNA1 show clear similarity to those of other Luteoviridae, which is why it has been placed in this family. In contrast, while ORFs 1 and 2 of PEMV2 RNA resemble those of the luteoviruses, they are most closely related to the umbraviruses which, like PEMV2 RNA, lack structural genes. Thus PEMV2 has been placed in the Umbravirus genus. PEMV may have originated as a mixed infection of an umbravirus and a polerovirus, with the former RNA providing a movement protein gene that confers the ability to spread beyond the phloem, allowing mechanical transmission.

Serologic Relationships

Luteoviridae have been compared extensively by ELISA. They can be clustered into the following subsets based on high serological crossreactivity: (1) BYDV-MAV, BYDV-PAV and BYDV-SGV; (2) CYDV-RPV, BYDV-RMV and RGV; (3) SBDV, SCRLV and BLRV; and (4) TNDV, PLRV and TYTV. BWYV reacts at least slightly with antibodies to nearly all Luteoviridae. All antibodies to BWYV crossreact with BMYV.

Epidemiology

The spread of Luteoviridae depends primarily on the movement of aphids that carry them. The mere presence of a large population of aphids is not sufficient to predict virus spread. The species of aphid and the predominant strain of virus are important factors. For instance, if a large population of Sitobion avenae accumulates in an oat field infected only with CYDV-RPV, these aphids are unlikely to spread the virus because S. avenae is a poor vector for CYDV-RPV. Luteoviridae are spread by aphids that colonize their host, rather than those that exhibit short probing behavior before moving on. The aphid must feed on phloem tissue to acquire and spread the virus. Because the virus must circulate and then accumulate in the accessory salivary gland of the aphid, a latent period of 8–24 h is necessary between the time the virus is acquired and the time it can be transmitted.

Because the virus is persistent, aphids can travel thousands of miles in jet streams over several days, and still transmit the virus. This is important because crops can become infected by a different strain of the virus than is found in the weeds in or near the field. On the other hand, neighboring crops and weeds often serve as reservoirs. Irrigated corn, weeds and nonweedy wild grasses can serve as symptomless hosts of BYDV or CYDV, from which the viruses are transferred to wheat, barley or oat crops by aphids. The timing of aphid infestation is important. A relatively small population of aphids can cause significant damage by infecting a crop when seedlings are young. When older plants are inoculated, the disease causes less damage.

Transmission and Tissue Tropism

Aphid transmission

With the exception of PEMV, Luteoviridae are transmitted to plants only via aphid vectors. Protoplasts can be inoculated by electroporation and whole plants have been infected by inoculation with Agrobacterium harboring a full-length clone of the BWYV genome in the Ti plasmid. Thus, the aphid does not supply a factor required for infection, rather its feeding likely serves as a very efficient delivery system. Luteoviridae are transmitted in a persistent, circulative manner, i.e. they circulate in the hemocele of the aphid. Once an aphid acquires a luteovirus, that virus can be transmitted throughout the life of the aphid, even after moltings. Luteoviridae do not replicate in aphids.

Luteoviridae have highly specialized relationships with their aphid vectors. This allowed differentiation of BYDV/CYDV strains based on their predominant aphid vectors (Table 1). Heterologous encapsidation in mixed infections can allow transmission of a genomic RNA of one strain by a vector of another. This phenomenon explains transmission of some virus complexes. CRLV allows the non-Luteoviridae carrot mottle umbravirus (CMoV) to be transmitted by Cavariella aegopodii in a persistent fashion because some CMoV genomic RNAs are encapsidated in particles containing CRLV coat protein. Similarly, groundnut rosette umbravirus is not transmissible in the absence of groundnut rosette assistor virus (GRAV) which, by itself, causes little damage.

The mechanism of virus transmission and vector specificity has been examined ultrastructurally by Gildow. He showed that the virus is specifically transported across three barriers: the hindgut epithelium, and the basal lamina and plasmalemma of the accessory salivary gland. Particles are then released into the phloem via the salivary duct as the aphid feeds. The particles appear to cross both the hindgut epithelium and the accessory salivary gland plasmalemma via receptor-mediated endocytosis in coated vesicles. Luteoviridae, but not other plant viruses, can cross the hindgut into the hemocele even in nonvector aphid species. However, only those virions that can be transmitted by the aphid can cross the plasmalemma of the accessory salivary gland. A highly abundant protein, called symbionin, that is produced by endosymbiotic bacteria (Buchnera spp.) in the hemocele, binds the readthrough domain of the virus particle. This protein resembles the chaperonin groEL, and may be involved in maintaining particle stability in the hemolymph.

Tissue tropism

Luteoviridae are generally confined to the phloem, including phloem parenchyma, companion cells and sieve elements. The exception is PEMV which can infect mesophyll cells and spread systemically, allowing it to be transmitted mechanically. The blockage of sieve tubes and degeneration of vascular tissue may account for the disease symptoms, although severity of disease symptoms does not always correlate with the amount of virus accumulating in the plant. Under laboratory conditions, protoplasts derived from mesophyll, epidermis, xylem and undifferentiated tissue can be infected with Luteoviridae. Thus, Luteoviridae do not require conditions found only in phloem cells, but rather their limitation to the phloem may be a result of their lack of ability to move from cell-to-cell into other tissues. Some evidence indicates that in whole plants, PLRV can be found in low levels in mesophyll cells.

Pathogenicity

Symptomatology

Symptoms caused by Luteoviridae are often difficult to identify clearly. In general, Luteoviridae cause stunting of plants, yellowing, reddening or ‘rolling’ of leaves, and an increase in leaf brittleness. Because symptoms may be confined to stunting or a change in leaf color that is not an obvious mosaic or mottle, luteovirus infection can be confused with nutritional deficiencies or other environmental stresses. Environmental factors also affect symptoms. Cool temperatures and high light maximize changes in leaf color. The most common symptom caused by BYDV or CYDV is stunting. As their names imply, they cause yellowing in many lines of barley. They can induce bright reddening of leaf tips in oats, corn and other grasses. This can be confused with the effects of frost. In oats, BYDV causes a marked increase in sterile florets. This, combined with reduced kernel weight caused by BYDV in oats and barley, greatly reduces grain yield. Symptoms can vary between hosts. A BYDV isolate called PAV129 is virtually symptomless in wheat from which it was isolated initially, but it is very severe in oats, including cultivars that are resistant to other isolates. BWYV induces bright yellowing of leaves on sugar beets, lettuce and spinach. In addition to leaf curling, PLRV causes net necrosis, a blackening of the vascular tissue in the tuber. Unlike most plant viruses, TNDV can kill its host in natural infections, as can BYDV under laboratory conditions.

Cytopathology

The cytopathology of Luteoviridae has been characterized best for BYDV and BWYV. Cells infected by luteoviruses show: (1) extreme distortion of the nucleus, and aggregation and accumulation of densely staining, heterochromatin-like material; (2) accumulation of new virus particles in the cytoplasm; and (3) single-membraned vesicles containing fibrils in the cytoplasm. Cells infected by poleroviruses show: (1) relatively normal nuclei at first, until the heterochromatin slowly disintegrates; (2) accumulation of new virus particles around the nucleolus; and (3) cytoplasmic vesicles containing fibrils enclosed in a second membrane.

Prevention and Control

Several strategies have been used to manage Luteoviridae. These include: (1) avoidance of aphids through careful monitoring of aphid populations and timing of planting; (2) use of insecticides or parasites to reduce aphid populations; and (3) use of crops that are genetically resistant to Luteoviridae. For control of BMYV in England, an equation involving the abundance of vector Myzus persicae in the autumn and the number of frost days in the winter is used to predict the arrival of aphids the following spring. If the predicted infestation is high, seeds pretreated with insecticide are recommended. An additional spray warning system is used after aphids have begun to colonize plants. If aphids exceed a threshold, growers are advised to spray insecticides. For BYDV hosts, sowing fall and spring cereals after major aphid migrations will reduce the chances of aphid colonization. However, this strategy reduces the time available for the crop to reach maturity and thus may reduce yield. The use of insecticides to control Luteoviridae is cost-effective only in areas of extremely intensive agriculture, such as wheat fields in England and potato fields in the northwestern USA. Parasitic wasps have proved to be effective biological control agents, reducing BYDV spread in South America, but their ability to control aphids is often limited.

A BYDV resistance gene, Yd2, from Ethiopian barley has been introduced into some commercial lines of barley. This has greatly reduced losses in California and elsewhere. However, this resistance has broken down in some cases, and is linked to undesirable traits. Tolerance to BYDV in oats is a quantitative trait. Resistance to BYDV has been introduced into wheat from Thinopyron species by alien gene introgression. However, the lines obtained to date still carry too many nonagronomic traits from the wild relative to be released as agronomically acceptable seed.

Plants that have been genetically engineered to express the coat protein of PLRV show delayed disease development and reduced symptoms when challenged with PLRV. Highly virus resistant Russet Burbank potatoes and oats have been obtained by transformation with the polymerase genes (ORFs 1 and 2) of PLRV and BYDV, respectively. Owing to the recombinogenic nature of the Luteoviridae genome on an evolutionary time scale, and the potential synergistic interactions between genomes, forethought must be used in designing and deploying Luteoviridae genes as resistance transgenes.

Economic Significance

The Luteoviridae family is one of the more economically significant plant virus families because BYDV, CYDV, PLRV and BWYV are ubiquitous, and cause significant losses in major crops. Because they often occur every year and are often not diagnosed, it is impossible to put an accurate dollar value on the losses due to Luteoviridae. Natural BYDV infection can cause average annual losses of 11–33%, and in some areas up to 86%. If BYDV caused 5% losses in 1989, it would have been valued at $US387 million for wheat, $US48 million for barley and $US28 million for oats. BYDV usually causes more obvious damage to oats and barley than to wheat. But due to the extensiveness of wheat production, the reduction in yield caused by BYDV, however slight, probably adds up to a significant monetary loss. The losses to BYDV in wheat are probably greater in North Africa, China and in tropical regions.

Infection of sugar beet with BMYV at an early stage in plant development can decrease root yield by 30%. Losses valued as high as £13000000 occur in BMYV epidemics in the UK. BWYV caused increasingly severe damage to sugar beets in California between 1951 and 1968. Beginning in 1968, the use of more resistant varieties of sugar beets and phytosanitary cropping practices greatly reduced the incidence of BWYV infection. The ensuing increase in yield, credited largely to the reduction in BWYV incidence, was estimated at $US167 million for a 5 year period in the state of California alone. Artificial inoculation of oilseed rape with BWYV resulted in 25% yield loss. BWYV has also been reported to cause significant losses in spinach, lettuce, turnips, cabbage, many brassicas, pea and flax at various locations around the world.

Groundnut rosette disease, caused by the complex of groundnut rosette virus and GRAV, is one of the most severe limitations to peanut production in Africa. The net necrosis symptom of PLRV makes potatoes unmarketable. Thus, yield loss in infected plants can be 100%. The value of the losses is so high that growers are anticipated to be willing to pay a premium for commercially produced transgenic potatoes with engineered resistance to PLRV. This, combined with engineered resistance to other viruses and insects in this potato variety, should reduce the need to apply high levels of insecticides that are currently used to control the aphid vector of PLRV and other insect pests.

See also:

Dianthoviruses (Tombusviridae); Pea Enation Mosaic Virus (Luteoviridae); Satellite RNAs and Satellite Viruses; Sobemoviruses; SYNERGISM | Plant Viruses; Umbraviruses; VECTORS | Plant Viruses.