R. W. Fulton
Department of Plant Pathology, University of Wisconsin, Madison, WI 53706, USA
Tobacco streak virus
Three or more types of quasi-isometric particle, c.
30 nm in diameter, which sediment
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
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:
||Description No. or
|Particle sizes (nm)
||Protein M. Wt (x 10-3)
||Tobacco streak (TSV)
||90, 98, 113
||27, 30, 35
||Asparagus virus II (AsV II)
||90, 95, 104
||26, 28, 32
||Citrus leaf rugose (CLRV)
||79, 89, 98, 105
||25, 26, 31, 32
||Citrus variegation (CVV)
||79, 83, 93, 110
||28, 31, 33
||Elm mottle (EMV)
||83, 88, 101
||Tulare apple mosaic (TAMV)
||93, 108, 114
||28, 30, 31
||Prunus necrotic ringspot (PNRSV)
||72, 90, 95
||Apple mosaic (ApMV)
||88, -, 117
||Prune dwarf (PDV)
||75, 81, 85, 99, 113
||20, 23, 19x33, 19x38
||Lilac ring mottle (LRMV)
||Spinach latent (SLV)
||87, 98, 108
||American plum line pattern (AmPLV)
||95, 100, 114, 126
||26, 28, 31, 33
(a) Uyeda & Mink (1981);
(b) Bos, Huttinga & Maat (1980);
(c) Fulton (1982).
Geographical Distribution etc
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.
Association with 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
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
Many ilarviruses are transmitted through seed. PNRSV,
the black raspberry latent strain of TSV,
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
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
). 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
germinates to produce plants without necrotic symptoms. No inclusion bodies have been described.
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
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
Purified preparations of several ilarviruses retain infectivity best in the
presence of EDTA
Halk & Fulton, 1978
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
daltons (RNA-4) or by its translation product, the coat protein
(Van Vloten-Doting, 1975
Gonsalves & Garnsey, 1975a
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
Relationships within the Taxon
Two subgroups were proposed by
Shepherd et al. (1975/76)
Subgroup A comprised
black raspberry latent virus. Subgroup B comprised
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
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
Rose mosaic and hop A viruses seem
to be closely related to ApMV
whereas cherry rugose mosaic, hop C,
Stecklenburg and Danish plum line pattern viruses seem to be closely related to PNRSV
Nyland & Lowe, 1964
Affinities with Other GroupsVan Vloten-Doting et al. (1981)
proposed that Ilarvirus
be considered a genus within
a family, Tricornaviridae. The other genera in the family would be
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)
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
(Hull, Hills & Markham, 1969
alfalfa mosaic virus also differs in having an
- Barbara, Clark, Thresh & Casper, Ann. appl. Biol. 90: 395, 1978.
- Bock, Ann. appl. Biol. 59: 437, 1967.
- Bos, Huttinga & Maat, Neth. J. Pl. Path. 86: 79, 1980.
- Casper, Phytopathology 63: 238, 1973.
- Cation, Phytopathology 39: 37, 1949.
- Converse & Lister, Phytopathology 59: 325, 1969.
- Davidson & George, Can. J. Pl. Sci. 44: 471, 1964.
- Fritzsche & Kegler, TagBer. dt. Akad. LandwWiss. Berl. 97: 289, 1968.
- Fulton, Phytopathology 58: 635, 1968.
- Fulton, Phytopathology 72: 1345, 1982.
- George & Davidson, Can. J. Pl. Sci. 43: 276, 1963.
- Gilmer, Pl. Dis. Reptr 39: 727, 1955.
- Gonsalves & Fulton, Virology 81: 398, 1977.
- Gonsalves & Garnsey, Virology 67: 311, 1975a.
- Gonsalves & Garnsey, Virology 67: 319, 1975b.
- Halk & Fulton, Virology 91: 434, 1978.
- Hampton, Phytopathology 56: 650, 1966.
- Hampton & Fulton, Virology 13: 44, 1961.
- Hull, Hills & Markham, Virology 37: 416, 1969.
- Jones & Mayo, Ann. appl. Biol. 79: 297, 1975.
- Kaiser, Wyatt & Pesho, Phytopathology 72: 1508, 1982.
- Lister & Saksena, Virology 70: 440, 1976.
- Mink, Virology 26: 700, 1965.
- Proeseler, Phytopath. Z. 63: 1, 1968.
- Nyland & Lowe, Phytopathology 54: 1435, 1964.
- Shepherd, Francki, Hirth, Hollings, Inouye, Macleod, Purcifull, Sinha, Tremaine & Valenta, Intervirology 6: 181, 1975/76.
- Swenson & Milbrath, Phytopathology 54: 399, 1964.
- Uyeda & Mink, Phytopathology 71: 1264, 1981.
- Uyeda & Mink, Phytopathology 73: 47, 1983.
- Van Vloten-Doting, Virology 65: 215, 1975.
- Van Vloten-Doting, Francki, Fulton, Kaper & Lane, Intervirology 15: 198, 1981.