Details of DPV and References

DPV NO: 275 July 1983

Species: | Acronym:

Ilarvirus group

R. W. Fulton Department of Plant Pathology, University of Wisconsin, Madison, WI 53706, USA


Type Member

Tobacco streak virus

Main Characteristics

Three or more types of quasi-isometric particle, c. 30 nm in diameter, which sediment at c. 80-90, 89-98 and 101-104 S. Particles of each type contain approximately the same proportion of nucleic acid and protein; differences in sedimentation rate are caused by differences in size of the particles. In some members, some of the fastest sedimenting particles are bacilliform. The genome of the viruses is distributed among three RNA species, with M. Wt ( x 10-6) of 1.1-1.3 (RNA-1), 0.9-1.1 (RNA-2) and 0.7-0.9 (RNA-3). All of these, plus either an RNA species of M. Wt 0.3 x 106 (RNA-4), which is a subgenomic fragment of RNA-3, or coat protein, which is a translation product of RNA -4, are required for infectivity. The small RNA or coat protein can be supplied by some, but not all, other ilarviruses or by alfalfa mosaic virus. Protein M. Wts reported are between 19,000 and 30,000, with most c. 25,000. Particles of some members are very unstable in plant sap unless an antioxidant is present, and their infectivity may be lost completely in 9-12 h; those of others retain infectivity in sap for a week or more at 22-24°C. Thermal inactivation points range from 42°C to 65°C. Most ilarviruses have wide host ranges; many infect woody plants. All can be transmitted by inoculation of sap, but virus concentration in leaf tissue may be low, so that transmision from woody to herbaceous hosts may depend on judicious selection of source tissue (young leaves, petals) from recently infected plants. Many ilarviruses are transmitted through seed; several are transmitted through pollen to the pollinated plant.


The definitive and provisional members of the group with some of their properties are:

    Virus Description No. or
of particles
Particle sizes (nm) Protein M. Wt (x 10-3)
Sub-group I
Tobacco streak (TSV) 44, 307 90, 98, 113 27, 30, 35 30
Sub-group II
Asparagus virus II (AsV II) a, 288 90, 95, 104 26, 28, 32 -
Citrus leaf rugose (CLRV) 164 79, 89, 98, 105 25, 26, 31, 32 26
Citrus variegation (CVV) 164 79, 83, 93, 110 28, 31, 33 26
Elm mottle (EMV) 139 83, 88, 101 25-30 25
Tulare apple mosaic (TAMV) 42 93, 108, 114 28, 30, 31 19
Sub-group III
Prunus necrotic ringspot (PNRSV) 5 72, 90, 95 c. 23 25
Apple mosaic (ApMV) 83 88, -, 117 25, 29 25
Prune dwarf (PDV) 19 75, 81, 85, 99, 113 20, 23, 19x33, 19x38 24
Lilac ring mottle (LRMV) 201 83, 98 avg 27 -
Spinach latent (SLV) b, 281 87, 98, 108 avg 27 28
American plum line pattern (AmPLV) c, 280 95, 100, 114, 126 26, 28, 31, 33 -

(a) Uyeda & Mink (1981); (b) Bos, Huttinga & Maat (1980); (c) Fulton (1982).

Geographical Distribution

The geographical distributions of ilarviruses infecting woody horticultural plants are apparently identical with those of their hosts as a result of their dissemination in vegetative propagating material as well as in seeds. Several others are distributed nearly world-wide in a variety of hosts, but a few are restricted to specific localities.

Transmission by Vectors

In spite of extensive trials with PNRSV, Swenson & Milbrath (1964) found no insect or mite vectors. However, transmission of PNRSV by the mite Vasates fockeui was reported by Proeseler (1968), and transmission by the nematode Longidorous macrosoma was reported by Fritzsche & Kegler (1968), but it is not known whether these vectors have any biological importance. No vectors have been reported for most other ilarviruses, but TSV was reported to be transmitted by either or both of two thrips species, Thrips tabaci and Frankliniella occidentalis (Kaiser, Wyatt & Pesho, 1982).

Ecology and Control

Many ilarviruses are transmitted through seed. PNRSV, the black raspberry latent strain of TSV, and PDV are also transmitted through pollen to the pollinated plant (George & Davidson, 1963; Converse & Lister, 1969). Field spread of PNRSV and PDV seems not to occur until their hosts reach flowering age (Davidson & George, 1964). These viruses are transmitted through seed as well and have probably been distributed with seed in commercial practice (Gilmer, 1955).

Relations with Cells and Tissues

Complete invasion of woody hosts may require more than 1 year, so that virus-free buds may be found on trees 1 to 2 years after the initial infection (Hampton, 1966). Invasion of herbaceous hosts is more rapid. Necrotic ‘shock’ symptoms occur when virus invades healthy tissue. Leaves produced subsequently show less severe symptoms, or none, and woody plants may show none in subsequent years. The ‘recovered’ leaves, however, contain virus. Virus-infected seed of Prunus spp. germinates to produce plants without necrotic symptoms. No inclusion bodies have been described.

Properties of Particles

Definitive ilarviruses have coat protein subunits of c. 25,000-28,000 M. Wt. Electron microscopic evidence indicates that the particles of unstable ilarviruses are easily deformed; unless fixed with glutaraldehyde they appear disrupted in negatively stained preparations. Some ilarviruses have quasi-isometric particles differing in size, but not in proportion of nucleic acid. Others, such as PDV, have a minor proportion of particles that are bacilliform. The unstable ilarviruses lose infectivity rapidly in crude sap by reaction with o-quinones formed by oxidation (Hampton & Fulton, 1961; Mink, 1965). Purified preparations of several ilarviruses retain infectivity best in the presence of EDTA (Fulton, 1982; Halk & Fulton, 1978).

Genome Properties

For those ilarviruses adequately investigated, the genome is tripartite, one part being contained in each of the three main particle types. The requirement for three or more particles to initiate infection results in a steep, multiple-hit dilution-infectivity curve. Pseudo-recombinants can be constructed by inoculating mixtures of the separated nucleoprotein components of strains with contrasting characters. The three main RNA species have M. Wt (x 10-6) of 1.1-1.3, 0.9-1.1 and 0.7-0.9.


Ilarviruses apparently replicate in the cytoplasm. To initiate infection the three genomic RNA species (RNA-1, RNA-2 and RNA-3) must be accompanied by a fourth, subgenomic, RNA of about 0.3 x 106 daltons (RNA-4) or by its translation product, the coat protein (Van Vloten-Doting, 1975; Gonsalves & Garnsey, 1975a, 1975b). The three genomic RNA species of TSV can be activated by RNA-4 or coat protein of alfalfa mosaic virus. Similarly the genomic RNA species of rose mosaic virus ApMV) can be activated by the RNA-4, or by the coat proteins, of PNRSV, CLRV or alfalfa mosaic virus (Gonsalves & Fulton, 1977).


Two subgroups were proposed by Shepherd et al. (1975/76). Subgroup A comprised TSV, TAMV, EMV, CLRV, CVV and black raspberry latent virus. Subgroup B comprised PNRSV and PDV. Uyeda and Mink (1983) proposed subdividing group A into the subgroups I and II shown in Table 1. Subgroup I contains TSV; black raspberry latent virus (Descr. No. 106) was also included here but it is serologically related to TSV and is now considered a strain (Jones & Mayo, 1975). Subgroup II comprises AsV II, CLRV, CVV, EMV and TAMV, which are also serologically interrelated. Subgroup B seems best re-named sub-group III and now comprises PDV, PNRSV and ApMV. The two last-named viruses cross-react with each other's antisera and have been considered serotypes (Barbara et al., 1978); at least one isolate seems to be intermediate between the two serotypes (Casper, 1973). Rose mosaic and hop A viruses seem to be closely related to ApMV (Bock, 1967; Fulton, 1968) whereas cherry rugose mosaic, hop C, almond calico, Stecklenburg and Danish plum line pattern viruses seem to be closely related to PNRSV (Fulton, 1968; Nyland & Lowe, 1964).

Affinities with Other Groups

Van Vloten-Doting et al. (1981) proposed that Ilarvirus be considered a ‘genus’ within a ‘family’, Tricornaviridae. The other genera in the family would be Bromovirus and Cucumovirus. Common characteristics are the tripartite RNA genomes and the existence of subgenomic RNA of 0.3-0.4 x 106 daltons. These authors, as well as Lister & Saksena (1976) and Gonsalves & Fulton (1977) have suggested that alfalfa mosaic virus be considered a member of the ilarvirus group on the basis of its tripartite genome and the ability of its protein or RNA-4 to activate the three genomic RNA species of some ilarviruses, and the capacity of its genomic RNA species to be activated by RNA-4 or protein of some ilarviruses. However, its particles are more markedly heterogeneous in morphology than those of most ilarviruses and they seem to have a more regular geometry (Hull, Hills & Markham, 1969); alfalfa mosaic virus also differs in having an aphid vector.


References list for DPV: Ilarvirus group (275)

  1. Barbara, Clark, Thresh & Casper, Ann. appl. Biol. 90: 395, 1978.
  2. Bock, Ann. appl. Biol. 59: 437, 1967.
  3. Bos, Huttinga & Maat, Neth. J. Pl. Path. 86: 79, 1980.
  4. Casper, Phytopathology 63: 238, 1973.
  5. Cation, Phytopathology 39: 37, 1949.
  6. Converse & Lister, Phytopathology 59: 325, 1969.
  7. Davidson & George, Can. J. Pl. Sci. 44: 471, 1964.
  8. Fritzsche & Kegler, TagBer. dt. Akad. LandwWiss. Berl. 97: 289, 1968.
  9. Fulton, Phytopathology 58: 635, 1968.
  10. Fulton, Phytopathology 72: 1345, 1982.
  11. George & Davidson, Can. J. Pl. Sci. 43: 276, 1963.
  12. Gilmer, Pl. Dis. Reptr 39: 727, 1955.
  13. Gonsalves & Fulton, Virology 81: 398, 1977.
  14. Gonsalves & Garnsey, Virology 67: 311, 1975a.
  15. Gonsalves & Garnsey, Virology 67: 319, 1975b.
  16. Halk & Fulton, Virology 91: 434, 1978.
  17. Hampton, Phytopathology 56: 650, 1966.
  18. Hampton & Fulton, Virology 13: 44, 1961.
  19. Hull, Hills & Markham, Virology 37: 416, 1969.
  20. Jones & Mayo, Ann. appl. Biol. 79: 297, 1975.
  21. Kaiser, Wyatt & Pesho, Phytopathology 72: 1508, 1982.
  22. Lister & Saksena, Virology 70: 440, 1976.
  23. Mink, Virology 26: 700, 1965.
  24. Proeseler, Phytopath. Z. 63: 1, 1968.
  25. Nyland & Lowe, Phytopathology 54: 1435, 1964.
  26. Shepherd, Francki, Hirth, Hollings, Inouye, Macleod, Purcifull, Sinha, Tremaine & Valenta, Intervirology 6: 181, 1975/76.
  27. Swenson & Milbrath, Phytopathology 54: 399, 1964.
  28. Uyeda & Mink, Phytopathology 71: 1264, 1981.
  29. Uyeda & Mink, Phytopathology 73: 47, 1983.
  30. Van Vloten-Doting, Virology 65: 215, 1975.
  31. Van Vloten-Doting, Francki, Fulton, Kaper & Lane, Intervirology 15: 198, 1981.