Details of DPV and References

DPV NO: 339 September 1988

Family:

Genus:

Species: | Acronym:

Includes viruses in the genera Luteovirus and Polerovirus and those in the family Luteoviridae not yet assigned to a genus.

Luteovirus group

P. M. Waterhouse Division of Plant Industry, CSIRO, Canberra, Australia

F. E. Gildow Department of Plant Pathology, Pennsylvania State University, USA

G. R. Johnstone Tasmania Department of Agriculture, Hobart, Australia

Contents

Type Member

Barley yellow dwarf virus - strain MAV.

Main Characteristics

Isometric particles c. 25 nm in diameter sedimenting as a single component at c. 104-118 S, and with a buoyant density in CsCl of c. 1.40 g/cm³. The protein shell is composed of one polypeptide species of M. Wt c. 24 x 10³ and the genome is a single molecule of positive sense, single-stranded RNA (M. Wt c. 2.0 x 10⁶). Luteovirus particles have high A₂₆₀/A₂₈₀ ratios of c. 1.6-1.9, are moderately stable (thermal inactivation points of 45-75°C), and are strongly immunogenic. Most members are serologically inter-related.

The name luteovirus (Latin, luteus = yellow) was coined because infected plants tend to show yellowing symptoms. Other characteristic symptoms are reddening, leaf curling, leaf rolling and brittleness. The concentration of virus particles within the plant is low (less than 100 µg/l of sap) and particles have been observed only in phloem tissues. Luteoviruses are transmitted neither by mechanical inoculation nor through seed, but are transmitted by aphids in a persistent (circulative, non-propagative) manner. Most members show a high degree of vector specificity and some luteoviruses can act as helpers for the aphid-transmission of associated viruses. The International Committee on Taxonomy of Viruses defined the luteovirus group in 1975 (Shepherd et al., 1976). It has since been reviewed by Duffus (1977b), Francki et al. (1985) and Rochow & Duffus (1981).

Members

Definitive and tentative members of the group are listed in Table 1. Those listed as possible or probable members resemble definitive luteoviruses in symptom expression and in their aphid transmission characteristics but are not sufficiently well studied to be classified unequivocally. Until recently, subterranean clover stunt virus was tentatively classified as a luteovirus. However, we exclude it from the group because its genome appears to be single-stranded DNA (Chu & Helms, 1987).

Table 1(a) Properties of definitive members of the luteovirus group (probable strains or synonyms are shown in italics and preceded by = )

	Main host family†	Main vector	Particle diam. (nm)	Genome RNA M. Wt (× 10-6)	Particle protein M. Wt (× 10-3)	A260/A280	s20,w	Density in CsCl (g/cm3)	DPV no. or reference
Barley yellow dwarf (BYDV)-MAV
	Gr	Sitobion avenae	26, 30, 24T	1.85	23.5	1.88-1.92	115-118	1.39	32; a-d
= (BYDV-PAV)
	Gr	S. avenae, Rhopalosiphum padi	26, 24T	2.0	24.4	1.76	115	1.40	32; a-d
= (BYDV-SGV)
	Gr	Schizaphis graminum	24T						32
Barley yellow dwarf (BYDV)-RPV
	Gr	R. padi	26, 30, 24T	1.85-2.0	24.4	1.71-1.79	115-118		32; a-d
= Rice guillaume (RGV)
	Gr	R. padi	28						e
= BYDV-RMV
	Gr	R. maidis	24T						32
Bean leaf roll (BLRV)
	Le	Acyrthosiphon pisum	27, 23T	2.4	23	1.83		1.32*	286
= Legume yellows (LYV)
	Le	Acyrth. pisum							f
= Michigan (lucerne) alfalfa (MiAV)
	Le	Acyrth. pisum							g
= Pea leaf roll
	Le	Acyrth. pisum							h
Beet western yellows (BWYV)
	Am, Ch, Co, Cr, Le, So	Myzus persicae	27, 26T	1.9	24				89; i; j
= Beet mild yellowing (BMYV)
	Ch, Cr	M. persicae	26	2.0	24-25.4	1.8	116	1.42	k, l
= Malva yellows (MYV)
	Ch, Co, Cr, Ma, So	M. persicae							m
= Turnip mild yellows (TuYV)
	Co, Cr	M. persicae							n
Carrot red leaf (CRLV)
	Um	Cavariella aegopodii	25	1.8	25	1.62	104	1.39	249
Groundnut rosette assistor (GRAV)
	Le	Aphis craccivora	28-30	2.1	24	1.86	115	1.34*	o, p
Indonesian soybean dwarf (ISDV)
	Le	Aphis glycines	26, 24T						q
Potato leafroll (PLRV)
	Am, So	M. persicae	24-25	2.0	26.3	1.78	115-127	1.39; 1.32*	36; 291
= Solanum yellows (SYV)
	So	M. persicae	28-30						r
= Tomato yellow top (TYTV)
	So	M. persicae	24		25.7			1.34*	s
Soybean dwarf (SDV)
	Le	Aulacorthum solani	25		22	1.96-1.90			179
= Subterranean clover red leaf (SCRLV)
	Le	Aul. solani	25	2.0	22.6	1.85	114		t, u
= Strawberry mild yellow edge (SMYEV)
	Fragaria spp.	Chaetosiphon fragaefolii	23						v, w
Tobacco necrotic dwarf (TNDV)
	So	M. persicae	25	2.0	25.7	1.8	115		234

 

Table 1(b) Probable and possible members of the luteovirus group

Probable members	Main host family†	Main vector species	Comments	Reference
Banana bunchy top (BBTV)	Musa spp.	Pentolonia nigranervosa	Double-stranded RNA profile typical of a luteovirus	x
Milk vetch dwarf	Le	A. craccivora	Isometric particles purified and seen in thin sections of phloem tissue	y
Millet red leaf	Gr	R. maidis, S. avenae, Sch. graminum	Possibly a form of BYDV	z
Physalis mild chlorosis	Cr, So	M. persicae	Possibly a form of BWYV	aa
Tobacco vein distorting (TVDV)	So	M. persicae	Acts as a helper virus	bb
Tobacco yellow vein assistor (TYVAV)	So	M. persicae	Acts as a helper virus	cc
Tobacco yellow net	So	M. persicae		dd
Possible members
Beet yellow net	Ch	M. persicae		ee
Celery yellow spot	Um	R. conii		ff
Cotton anthocyanosis	Ma	Aphis gossypii		gg
Filaree red leaf	Geraniaceae	Acyrth. pe!argonii		hh
Grapevine ajinashika	Vitis spp.	Vector unknown		ii
Physalis vein blotch	So	M. persicae		jj
Raspberry leaf curl	Rosaceae	Aphis rubicola		kk

T= Measurement of particles seen in thin sections. * = Buoyant density in caesium sulphate solutions. † Abbreviations for family names: Am Amaranthaceae; Ch Chenopodiaceae; Co Compositae; Cr = Cruciferae; Gr = Gramineae; Le = Leguminosae; So = Solanaceae; Ma = Malvaceae; Um = Umbelliferae.

References: a: Brakke & Rochow, 1974; b: Scalla & Rochow, 1977; c: Paliwal, 1978; d: Hammond et al., 1983; e: Amici et al., 1978; f: Duffus, 1979; g: Thottappilly et al., 1977; h: Hampton, 1983; i: Falk et al., 1977; j: Falk & Duffus, 1984; k: Chevallier et al., 1983; l: Govier, 1985; m: Costa et al., 1959; n: Watson, 1964; o: Casper et al., 1983; p: Rajeshwari & Murant, 1988; q: Iwaki et al., 1980; r: Milbrath & Duffus, 1978; s: Thomas, 1984; t: Johnstone et al., 1982; u: Ashby & Kyriakou, 1983; v: Martin & Converse, 1985; w: Spiegel et al., 1986; x: Dale et al., 1986; y: Inouye et al., 1979; z: Yu et al., 1957; aa: MacKinnon, 1965; bb: Smith, 1946; cc: Adams & Hull, 1972; dd: Sylvester, 1954; ee: Sylvester, 1948; ff: Freitag & Severin, 1945; gg: Costa, 1957; hh: Frazier, 1951; ii: Namba et al., 1979; jj: MacKinnon & Lawson, 1966; kk: Bennett, 1930.

Geographical Distribution

Luteoviruses have been described from most parts of the world including tropical, sub-tropical and temperate regions. Many luteoviruses, including BYDV, BWYV, CRLV and PLRV, are widespread but others, such as TNDV, have restricted distributions. With the exception of BWYV and close serological relatives, all the definitive members have natural host ranges largely restricted to one plant family (Table 1).

Transmission by Vectors

Luteoviruses are transmitted in a persistent (circulative, non-propagative) manner. Aphids acquire and transmit luteoviruses while feeding on phloem sieve tube elements of host plants. Minimum feeding access times reported for aphids to acquire or inoculate different luteoviruses range from 0.1-4.0 h and 0.2-1.0 h respectively (Cockbain & Costa, 1973; Duffus, 1960, 1979; Elnagar & Murant, 1978; Thottappilly et al., 1977). These reported times include the time required for the aphids’ stylets to penetrate to the phloem tissues. Mean times for stylet penetration of sieve tube elements in oats were 200, 60 and 32 min for Schizaphis graminum, Rhopalosiphum padi and Sitobion avenae respectively (Montllor & Gildow, 1986; Scheller & Shukle, 1986). Electronic monitoring of Myzus persicae on potato showed that aphids whose stylets had penetrated and remained in sieve elements for a minium of 1-2 min subsequently became able to transmit PLRV (Leonard & Holbrook, 1978). Efficient transmission of most luteoviruses requires acquisition and inoculation feeding access times each of 24 h. The minimum latent period (usually defined as the time from the start of the acquisition feeding period until the insect becomes able to infect plants with the virus) is normally between 12 and 24 h (Duffus, 1977b; Elnagar & Murant, 1978; Rochow, 1963). Median latent periods (LP5O, time for 50% of the aphids to begin to transmit) are 35-50 h at 15-20°C for BYDV-RPV, 44-65 h at 15-20°C for BYDV-MAV (Van der Broek & Gill, 1980) and 30-49 h at 20-25°C for PLRV (Eskandari et al., 1979). Factors influencing luteovirus transmission were described by Sylvester (1980).

Aphids that have acquired a luteovirus do not cease to transmit it after moulting and studies of BYDV transmission by R. padi (Gildow, 1985) indicate that luteovirus particles pass by cellular transport through the hindgut into the aphid’s haemocoel. The particles then circulate in the haemolymph throughout the aphid. Current evidence indicates that luteoviruses do not replicate in their vectors (although Weidemann (1982) suggested that they may do so to a small extent), but aphids that have begun to transmit a luteovirus may continue to do so for 2-3 weeks without re-acquisition. Ultrastructural studies on BWYV, BYDV and PLRV suggest that they are transmitted following endocytosis of virus particles from the haemocoel into the aphid’s accessory salivary gland. The particles are then transported within coated vesicles through the salivary gland secretory cell, and released by exocytosis into the salivary duct (Gildow & Rochow, 1980a; Gildow 1982, 1987).

A characteristic feature of the luteoviruses is their high degree of vector specificity (Table 1). Each luteovirus is transmitted efficiently by only one or a few species of aphid. Vector specificity is believed to result from interactions between the particle protein and membrane surfaces in the aphid’s accessory salivary gland; these interactions regulate transport of virus particles to the salivary duct (Gildow & Rochow, 1980b). Vector specificity is not absolute, however, and some luteoviruses are transmitted inefficiently by species other than the main vector (Rochow, 1969). Transmission efficiency has also been reported to vary with the age of the aphid (Gill, 1970; Upreti & Nagaich, 1971; Zhou & Rochow, 1984), and among distinct populations or clones of a single aphid species (Bjorling & Ossiannilsson, 1958; Cockbain & Costa, 1973; Gildow & Rochow, 1983; Rochow, 1960). Genetic variability of aphids, as well as the viruses, evidently influences vector specificity and transmission efficiency.

Ecology and Control

Some luteoviruses may be disseminated with infected planting material, for example BBTV with banana suckers, PLRV with potato tubers, and SMYEV with strawberry runners. Clean stock schemes are operated in many parts of the world to control these viruses (Allen, 1983; Harrison, 1984; Mullin et al., 1974). Most other luteoviruses cause diseases in annual crops and are introduced each year by their aphid vectors. The viruses spread into the annual crops from reservoirs which include volunteer plants from the previous year's crop, other crops, alternative perennial hosts and weeds. In some instances, infective vectors may be transported long distances in wind currents (Fargette et al., 1982). Weeds are a particularly important source of BWYV infection, and perennial grasses and legumes are important reservoirs of BYDV and legume-infecting luteoviruses (SDV, BLRV, BWYV) respectively. The relative importance of secondary spread by apterae within a crop and of primary introductions by alatae varies with the virus, the vector species, the crop species and the climatic conditions. Organophosphate aphicides help control secondary spread of luteoviruses but are ineffective against primary introductions. In contrast, synthetic pyrethroids have a rapid knock-down property that can be useful in decreasing primary spread (Gibson et al., 1982; Johnstone, 1984). Other control approaches have included judicious choice of sowing date in relation to aphid flight activity (Stubbs, 1948), elimination of virus sources (Duffus, 1971), adoption of crop-free periods (Duffus, 1977a), crop production in isolation (Shepard & Claflin, 1975), breeding for various forms of virus resistance or tolerance (Barker & Harrison, 1985; Jedlinski et al., 1977; Schalter et al., 1963), breeding for resistance to aphid feeding (Gibson, 1977) and biological control of the aphid vector (Stubbs et al., 1983).

A number of luteoviruses occur in the field as part of a complex, either with other luteoviruses, such as BWYV and SDV in legumes (Johnstone & Duffus, 1984) and various BYDV serotypes in cereals (Rochow & Muller, 1974), or with members of other virus groups, as with the virus complexes found in strawberries (Prentice, 1946). Some viruses depend on luteoviruses for their aphid transmission (Table 2), for example carrot mottle virus depends on CRLV, and groundnut rosette virus depends on GRAV. These pairs of viruses occur as complexes that seem to be very stable and may show a synergistic effect with regard to symptoms.

Table 2. Luteoviruses which have a helper activity and their associated dependent virus

Helper virus	Vector	Dependent virus	Reference
BYDV-RMV	Rhopalosiphum maidis	BYDV-MAV	Rochow, 1975
BYDV-RMV	R. maidis	BYDV-RPV	Rochow, 1982
BYDV-RPV	R. padi	BYDV-MAV	Rochow, 1970
BYDV-RPV	R. padi	BYDV-RMV	Rochow, 1982
BYDV-RPV	R. padi	BYDV-SGV	Rochow, 1982
BYDV-PAV	R. padi	BYDV-RMV	Rochow, 1982
BYDV-PAV	R. padi	BYDV-MAV	Rochow, 1982
BLRV	Acyrthosiphon pisum	Bean yellow vein-banding	Cockbain, 1978; Cockbain et al., 1986
BWYV	Myzus persicae	Lettuce speckles mottle	Falk et al., 1979
BWYV*	M. persicae	Carrot mottle	Waterhouse & Murant, 1983
CRLV	Cavariella aegopodii	Carrot mottle	Watson et al., 1964
GRAV	Aphis craccivora	Groundnut rosette	Hull & Adams, 1968
GRAV*	A. craccivora	Tobacco yellow vein	Adams & Hull, 1972
PLRV*	M. persicae	Carrot mottle	Waterhouse & Murant, 1983
TVDV*	M. persicae	Tobacco yellow vein	Adams & Hull, 1972
TVDV	M. persicae	Tobacco mottle	Smith, 1945; 1946
TYVAV	M. persicae	Tobacco yellow vein	Adams & Hull, 1972
TuYV	M. persicae	Lettuce speckles mottle	Falk et al., 1979

* = Shown to act as a helper experimentally but not known to do so in nature.

Relations with Cells and Tissues

Luteoviruses are tissue-specific and replicate in phloem cells of plant hosts. Virus particles are detected most readily in sieve elements, companion cells, and occasionally in phloem parenchyma. Particles were found only in phloem transfer cells of SCRLV-infected subterranean clover (Jayasena et al., 1981). With one exception (Gill & Chong, 1981), luteoviruses have not been observed in epidermal, mesophyll or xylem tissues of infected plants. Evidence suggests that luteoviruses spread rapidly from cell to cell longitudinally through the vascular bundle; however, lateral spread is slow and not all phloem cells of a bundle may be infected (Jensen, 1969; Murant & Roberts, 1979). The primary symptom of infection is necrosis of the phloem (Esau, 1957), which spreads from the initially inoculated sieve element to adjacent cells. Phloem necrosis is associated with resistance to translocation of plant metabolites, loss of chlorophyll, increased respiration, and decreased growth (Goodman et al., 1965; Jensen, 1972; Orlob & Arny, 1961).

Ultrastructural examinations of infected plants have been reported for several luteoviruses (D’Arcy & De Zoeten, 1979; Esau & Hoefert, 1972; Faoro et al., 1978; Jayasena et al., 1981; Jensen, 1969; Kojima et al., 1969; Kubo, 1981; Murant & Roberts, 1979; Shepardson et al., 1980). The most detailed study was that of Gill & Chong (1979) on BYDV isolates infecting oats, and showed that at least two distinct sequences of events may be involved in replication of viruses assigned to the luteovirus group. Based on cytopathological ultrastructure involving alterations of the nucleus, site of virus accumulation and types of vesicles produced, these authors suggested dividing BYDV isolates into subgroup 1 (MAV, PAV, SGV) and subgroup 2 (RPV, RMV). In oats infected with isolates of subgroup 1, virus particles seem to move from sites of initial inoculation in sieve elements through plasmodesmata into adjacent companion cells. Densely staining filaments (2-4 nm diameter) and single membrane-bound vesicles (50-230 nm diameter) form in the cytoplasm near the plasmodesmata. Filaments are later observed within the nucleus, which becomes distorted and begins to deteriorate soon after infection. Virus particles are first observed to occur in the cytoplasm, suggesting a cytoplasmic site for assembly. At about this time the mitochondria, plastids and ribosomes begin to disintegrate. Isolates in subgroup 2 initiate infection of companion cells in a similar manner; however, the vesicles produced are bounded by a second membrane which is continuous with the endoplasmic reticulum. A second type of membrane system (composed of tubules) proliferates, and the dense filaments are rare in the cytoplasm and do not occur in the nucleus. The nucleus does not deteriorate and virus particles are first observed surrounding the nucleolus within the nucleus. In addition, extensive wall thickenings develop in the infected parenchyma cells.

Ultrastructural changes induced by BWYV and PLRV seem to be similar to those caused by BYDV isolates of subgroup 2 (Esau & Hoefert, 1972; Shepardson et al., 1980). However, cytopathological effects vary with host species and virus isolate (D'Arcy & De Zoeten, 1979; Gill & Chong, 1981; Kojima & Yanase, 1984).

Properties of Particles

Particles: Properties of luteovirus particles are summarised in Table 1. When negatively stained, most luteovirus particles have a diameter of c. 25-28 nm; they are usually angular in outline and not penetrated by stain. Thermal inactivation points range from 45°C to 75°C. The particle mass of BMYV is 6.5 x 10⁶, as determined by optical diffraction and scanning transmission electron microscopy (Chevallier et al., 1983). The protein subunits of a luteovirus particle are probably in a T = 3 arrangement: the M. Wt of 180 protein subunits plus the M. Wt of the RNA gives a total very close to that obtained for the whole particle mass of BMYV. Hewings & D’Arcy (1983) reported that purified preparations of a legume isolate of BWYV contained not only the usual nucleoprotein particles but also particles made of the viral protein subunits but devoid of nucleic acid. The isoelectric point of TNDV particles is 5.3 (Kubo, 1981).

Nucleic acid: The genomes of all luteoviruses so far analysed consist of single-stranded RNA with a M. Wt of c. 2.0 x 10⁶. The genome of PLRV was at first reported to be double-stranded DNA (Sarkar, 1976) but this has not been confirmed in more recent work (Rowhani & Stace-Smith, 1979; Takanami & Kubo, 1979b). The RNA molecules of PLRV, BYDV and CRLV each represent 28-30% of the particle weight (Harrison, 1984; Paliwal, 1978; Waterhouse & Murant, 1982). One isolate of BWYV, but not others, has a second RNA component (M. Wt 0.86 x 10⁶) which was found to be associated with increased virulence (Falk & Duffus, 1984). However, this RNA component is probably not subgenomic (Falk & Anderson, 1987). The RNA extracted from TNDV particles also included two small RNA molecules (M. Wt 1 x 10⁵), but their origin and significance is presently unknown (Takanami & Kubo, 1979a,1979b).

An isolate of BYDV-RPV studied by Miller et al. (1987) has an associated small circular self-cleaving single-stranded RNA (351 nt) which has no homology with the viral genome and therefore appears to be satellite RNA.

Coat protein: The coat protein subunits of luteoviruses so far studied are all of M. Wt c. 24,000. The coat protein subunit of BLRV was originally reported to be c. 32,500 (Ashby & Huttinga, 1979) but a more recent estimate is c. 23,000 (R. O. Hampton, cited by Ashby, 1984). The amino acid composition of the coat protein subunits has been determined for only three luteoviruses: TNDV (Kubo, 1981), BYDV-PAV (P. M. Waterhouse & A. A. Kortt, unpublished data) and SDV (P. M. Waterhouse & A. A. Kortt, unpublished data):

		lys	his	arg	asp	thr	ser	glu	pro	gly	ala	cys	val	met	ile	leu	try	phe	trp
TNDV:		10	4	21	20	12	24	16	9	23	12	3	13	2	10	23	6	9	2
SDV:		15	4	17	23	15	23	19	10	24	16	1	12	1	13	13	6	11	0
BYDV:		12	2	19	19	17	19	15	8	23	17	1	12	3	11	9	5	4	nd

The relatively low amounts of aromatic amino acids (mainly tyrosine and tryptophan) in the coat protein subunits of TNDV, SDV and BYDV may well account for the unusually high A₂₆₀/A₂₈₀ ratios observed for particle preparations of these and some other luteoviruses.

Genome Properties

The RNA of PLRV (Mayo et al., 1982) is covalently bound to a genome-linked protein (M. Wt 7000) and has no substantial polyadenylate sequence. The luteovirus genome is probably positive sense: viral polypeptides have been synthesised by in vitro translation of the encapsidated RNA of PLRV and SDV. Translation of PLRV RNA in rabbit reticulocyte lysates gave polypeptides of M. Wt c. 125,000 and 71,000 (Mayo et al., 1982). In wheat germ extracts these two and an additional polypeptide (M. Wt 29,000) were obtained (Mayo & Barker, 1984). SDV RNA gave one predominant translation product (M. Wt c. 45,000-50,000) with either the rabbit reticulocyte or the wheat germ systems (Anon., 1984). None of the polypeptides produced from translation of either RNA was precipitated by antiserum against the homologous coat protein.

The complete nucleotide sequence of a BYDV-PAV serotype has been determined and its genome organization inferred from open reading frames (Miller et al., 1988a,1988b). The gene nearest to the 5' end encodes the RNA-dependent RNA polymerase, the coat protein gene is located near the middle of the genome and there is a possibility of translational readthrough from the coat protein gene to yield a 69 kd protein.

The nucleotide sequence of a satellite RNA associated with an isolate of BYDV-RPV is also known (Miller et al., 1987). It has been inferred from the sequence that the satellite RNA has a high degree of secondary structure and is not translated.

Replication

Little is known about the replication of luteoviruses. Although luteovirus particles are found only in phloem tissues, PLRV, TNDV and BYDV can replicate in mesophyll protoplasts (Barnett et al., 1981; Takanami & Kubo, 1979a) and SDV can replicate in soybean protoplasts derived from suspension cultures (Waterhouse & Gerlach, 1984). Furthermore, TNDV can replicate in inoculated epidermal cells (Imaizumi & Kubo, 1980). Therefore, the restriction of luteoviruses to cells of the phloem tissues is not because other cells are incapable of supporting their replication.

Subgenomic RNA species have been detected in nucleic acid extracts from PLRV-infected potato (M. Wt 1 x 10⁶; Barker et al., 1984) and from BYDV-PAV -infected oats (2.8 and 0.8 kb; Gerlach et al., 1987). Five species of double-stranded RNA have been extracted from tissue infected with BYDV-RPV (Gildow et al., 1983) or BWYV (Falk & Duffus, 1984) and four species from tissue infected with BYDV-MAV (Gildow et al., 1983). This information and the incomplete translation of PLRV or SDV RNA in vitro suggests that luteoviruses may be translated via subgenomic messenger RNA species.

Relationships

The definitive luteoviruses form a network of serological relationships (Fig. 1). BWYV is directly serologically related to almost all definitive members. Luteoviruses seem to form a serological continuum but with a degree of clustering. Thus BWYV, BMYV, MYV and TuYV form a cluster which we have grouped as isolates of BWYV; similarly BLRV, LYV and MiAV form a cluster, as do PLRV, SYV and TYTV plus possibly TNDV. Also, SDV and SCRLV are very close. These same clusters are also seen when examining host range and vector specificity (Table 1). Paradoxically, BYDV isolates form not one cluster but two, one containing MAV, PAV and SGV, and the other containing RPV and RMV. This division is also supported by cytopathology (Gill & Chong, 1979), dsRNA profile (Gildow et al., 1983), nucleic acid hybridization (Waterhouse et al., 1986) and cross-protection studies (Jedlinski & Brown, 1965) and we suggest that these two subgroups should be regarded as two different viruses, BYDV-MAV and BYDV-RPV. Little work has been done on the inter-relationship of luteoviruses at the nucleic acid level. However, cross hybridization has been detected between regions of the BYDV-PAV genome and regions of the BYDV-RPV, SDV, PLRV and BWYV genomes (Waterhouse et al., 1986).

Affinities with Other Groups

Apart from the luteoviruses, the only other plant virus that is transmitted in a circulative, non-propagative, manner is pea enation mosaic virus (considered to form a monotypic group). There are many similarities between PEMV and luteoviruses in vector relations, particle morphology and composition, and in the ability to act as a helper virus. However, PEMV has at least two RNA components and is manually transmissible.

Sequence homology has been detected in the polymerase gene of BYDV and that of carnation mottle virus and in the coat protein gene of BYDV and that of southern bean mosaic virus (Miller et al., 1988a, 1988b).

A number of luteoviruses can assist the aphid-transmission of dependent viruses such as carrot mottle virus (Table 2). It has been shown for two of these dependent viruses that their genomic RNA species can become encapsidated in the coat protein of the helper virus (Falk et al., 1979; Waterhouse & Murant, 1983), and this is thought to explain how they become transmissible by the aphid vector of the helper virus. It has also been shown that the dependent virus can change its helper virus and consequently its aphid vector (Adams & Hull, 1972; Waterhouse & Murant, 1983).

Figures

References list for DPV: Luteovirus group (339)

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31. Duffus & Russell, Phytopathology 62: 1274, 1972.
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36. Esau & Hoefert, Virology 48: 724, 1972.
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58. Gill & Chong, Virology 95: 59, 1979.
59. Gill & Chong, Virology 114: 405, 1981.
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68. Imaizumi & Kubo, Ann. phytopath. Soc. Japan 46: 54, 1980.
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72. Jedlinski & Brown, Virology 26: 613, 1965.
73. Jedlinski, Rochow & Brown, Phytopathology 67: 1408, 1977.
74. Jensen, Virology 38: 83, 1969.
75. Jensen, Phytopathology 62: 587, 1972.
76. Johnstone, in The Winston Churchill Memorial Trust - Fellowship Report, 110 pp., 1983.
77. Johnstone, Australas. Pl. Path. 13: 55, 1984.
78. Johnstone & Duffus, Aust. J. agric. Res. 35: 821, 1984.
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82. Kubo, CMI/AAB Descr. Pl. Viruses 234, 4 pp., 1981.
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89. Mayo & Barker, Rep. Scott. Crop Res. Inst., 1983: 186, 1984.
90. Mayo, Barker, Robinson, Tamada & Harrison, J. gen. Virol. 59: 163, 1982.
91. Milbrath & Duffus, Phytopath. News 12: 170, 1978.
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95. Montllor & Gildow, Entomologia exp. appl. 42: 63, 1986.
96. Mullin, Smith, Frazier, Schlegel & McCall, Phytopathology 64: 1425, 1974.
97. Murant & Roberts, Ann. appl. Biol. 92: 343, 1979.
98. Namba, Yamashita, Doi & Yora, Ann. Phytopath. Soc. Japan 45: 70, 1979.
99. Orlob & Arny, Phytopathology 51: 768, 1961.
100. Paliwal, Phytopath. Z. 92: 240, 1978.
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102. Rajeshwari & Murant, Ann. appl. Biol. 112: 403, 1988.
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104. Roberts, Tamada & Harrison, J. gen. Virol. 47: 209, 1980.
105. Rochow, Phytopathology 50: 881, 1960.
106. Rochow, Phytopathology 53: 355, 1963.
107. Rochow, Phytopathology 59: 1580, 1969.
108. Rochow, A. Rev. Phytopath. 10: 101, 1970.
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110. Rochow, Phytopathology 72: 302, 1982.
111. Rochow & Carmichael, Virology 95: 415, 1979.
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114. Rochow & Muller, Pl. Dis. Reptr 58: 472, 1974.
115. Rowhani & Stace-Smith, Virology 98: 45, 1979.
116. Sarkar, Virology 70: 265, 1976.
117. Scalla & Rochow, Virology 78: 576, 1977.
118. Schalter, Qualset & Rutger, Crop Sci. 4: 544, 1963.
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120. Shepard & Claflin, A. Rev. Phytopath. 13: 271, 1975.
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