375
June 2000
Family: Unallocated ssRNA- viruses
Genus: Tenuivirus
Species: Rice stripe virus
Acronym: RSV

This is a revised version of DPV 269

Rice stripe virus

S. Toriyama
Department of Microbiology, National Institute of Agro-Environmental Sciences, Kannondai 3, Tsukuba, Ibaraki 305-8604, Japan.

Contents

Introduction
Main Diseases
Geographical Distribution
Host Range and Symptomatology
Strains
Transmission by Vectors
Transmission through Seed
Transmission by Grafting
Transmission by Dodder
Serology
Nucleic Acid Hybridization
Relationships
Stability in Sap
Purification
Properties of Particles
Particle Structure
Particle Composition
Properties of Infective Nucleic Acid
Molecular Structure
Genome Properties
Satellites
Relations with Cells and Tissues
Ecology and Control
Notes
References
Acknowledgements
Figures

Introduction

Disease described by Kuribayashi (1931a). Virus characterized by S. Toriyama (1982a, 1982b, 1986) and S. Toriyama et al. (1994a).

A virus with filamentous particles, 500-2000 nm long, but only about 8 nm wide. The particles sediment as four components and contain four ssRNA species, a major protein (the nucleocapsid protein) and a minor protein (the RNA polymerase). RNA-1 is negative-stranded and RNAs 2 to 4 are ambisense. Non-structural protein material is produced abundantly in infected cells. Mechanical inoculation is difficult. The virus is transmitted by Laodelphax striatellus and three other planthopper species in a persistent manner; it is transmitted through the egg to about 90% of progeny insects. It infects many species of Gramineae. It occurs in rice-growing areas of Asia and the USSR, and causes significant reduction in rice yield.

Main Diseases

In rice the virus causes chlorotic stripes, chlorosis, moderate stunting and loss of vigour (Fig.1): in severe infections the leaves develop brown to grey necrotic streaks and die. Diseased plants produce few or no panicles: those produced carry whitish to brown discoloured malformed spikelets (Fig.2). Early infection of rice causes significant loss of yield (Yasuo, Ishii & Yamaguchi, 1965, Yasuo, 1969, Lee, 1969); late infection also reduces yield by retarding ear emergence and ripening (Yasuo et al., 1965). In maize and wheat the virus causes chlorotic stripes, chlorosis and stunting.

Geographical Distribution

The disease was first recognized in the early 1900s in central Japan, where severe damage was caused to rice crops. Since the 1950s the extension of early planting favoured the occurrence of the disease in Japan (Yasuo et al., 1965, Iida, 1969) and during the 1960s and 1970s about 200,000 ha of rice was affected each year. In Korea, the disease affected 40% of rice hills in 1965 (Lee, 1969). Stripe disease incidence in Taiwan was most severe around 1970: 1045 ha were affected in 1973 (Lee, 1975). Stripe disease is broadly prevalent all over the rice-growing areas in China (Chen, 1964, Lin et al., 1990) and the USSR (Reifman, Pinsker & Krylova, 1978).

Host Range and Symptomatology

RSV occurs naturally in rice, maize, wheat, oat, foxtail millet and wild grasses such as Cynodon dactylon, Digitaria adscendens, D. violascens, Eragrostis multicaulis and Setaria viridis. The virus is reported to infect 37 species of the family Gramineae. The main type of symptom induced is chlorotic striping (Kuribayashi, 1931a, 1931b; Amano, 1937; Shinkai, 1955, 1962; Yamada & Yamamoto, 1956; Sugiyama, 1966). Non-gramineous plant species, such as Cyperus amuricus var. laxus, C. sanguinolentus, and Eriocarlan robustius are also reported as host plants (Chung & Lee, 1971; Pinsker & Reifman, 1975). The virus is readily transmitted to test plants by the planthopper, Laodelphax striatellus, but is difficult to transmit mechanically. Okuyama & Asuyama (1959) obtained infection in 6% of plants that were injected with crude extracts made from diseased plants with 0.01 M cysteine-HCl, and Sonku (1973) achieved infection in 0.9% of plants that were injected with extracts of viruliferous insects.

Diagnostic species

Oryza sativa (rice). Seedlings of most Japanese paddy varieties are highly susceptible to infection. Chlorotic stripes, mostly light yellowish broken streaks (Fig.1), develop on systemically infected leaves 10 to 25 days after inoculation by planthoppers (L. striatellus). Characteristically, limp chlorotic leaves emerge without unfolding, elongate, droop and wilt (Fig.3). Yellowing and moderate stunting also occur.

Triticum aestivum (wheat) and Zea mays (maize) (cv. Golden Cross Bantam). Symptoms in these species are similar to those in O. sativa. Wheat plants may produce whitish, rolled, needle-like leaves that quickly droop.

Propagation species

Rice, wheat and maize are used to maintain cultures and as a source of virus for purification. Young rice seedlings are readily killed, and so care must be taken to use the appropriate growth stage and varieties, e. g. third leaf stage of rice cv. Norin No. 8 or Kinmaze. When maize seedlings are used, wheat, barley or rice plants must also be planted, or the planthoppers will die within 2-3 days.

Assay species

Young rice and wheat seedlings are suitable for assaying transmission by insect vectors.

Strains

An isolate that causes mild symptoms on rice (Ishii & Ono, 1966) and two variants that differ in symptoms induced in wheat and in insect transmissibility (Kisimoto, 1965) are reported. Also, Hayashi et al. (1989) found four isolates that produce disease-specific non-structural proteins of different molecular weights. However, there are no detailed studies of any of these isolates.

Transmission by Vectors

The most active vector in the field is the small brown planthopper, Laodelphax striatellus (Kuribayashi, 1931a, 1931b); three other planthopper species, Unkanodes sapporona (Shinkai, 1966), U. albifascia (Hirao, 1968) and Terthron albovittatum (Shinkai, 1970) also transmit. The proportion of active transmitters of L. striatellus is about 20% (Shinkai, 1962). Although the shortest acquisition feeding period is 15 min, best transmission is obtained with planthoppers that acquire the virus by feeding for 1 day. The incubation period of the virus in L. striatellus ranges from 5 to 21 days but incubation is complete within 5 to 10 days for most individuals. Minimum inoculation feeding time is 3 min: about half or more of the infective planthoppers infect rice seedlings after feeding for 1 h (Yamada &Yamamoto, 1955; Shinkai, 1962). Ability of the insects to transmit the virus decreases markedly with age. Females of L. striatellus are more efficient transmitters than males (Shinkai, 1962). The virus passes through a high percentage of eggs to progeny, about 90% in L. striatellus (Kuribayashi, 1931b; Yamada &Yamamoto, 1954, 1955; Shinkai, 1954, 1962). L. striatellus was selected and bred for high or low ability to acquire and transmit the virus (50-60% and less than 10% of the insects transmitting, respectively), and this was correlated with the frequency of transmission of the virus through the eggs (Kisimoto, 1967). Evidence of virus multiplication in L. striatellus has been obtained by repeated passage through the eggs for 6 years through 40 generations (Shinkai, 1962), by serial transfer of the virus from insects to insects by injection (Okuyama, Yora & Asuyama, 1968) and by detection of virus particle antigen in various organs of viruliferous insects with the fluorescent antibody staining technique (Kitani, Kiso & Yamamoto, 1968).

Transmission through Seed

None found in rice (Kuribayashi, 1931b; Okuyama, 1959).

Serology

RSV is a good immunogen. Rabbit antisera with titres of 1/512 to 1/1024 in precipitin tests are readily obtained. In agar gel diffusion tests, it is necessary to disrupt virus particles in purified preparations or crude sap of infected tissues by treatment with 0.5% SDS. The haemagglutination test was used to detect the virus particle antigen at high dilutions in vectors or plants (Saito & Iwata, 1964; Yasuo &Yanagita, 1963; Sonku & Sakurai, 1973b). Monoclonal antibodies have been made and used for specific detection of the viral antigen (Omura et al., 1986) and ELISA is useful for detecting the virus in plants and vectors (Omura et al., 1986; Y. Takahashi et al., 1987; Cheng et al., 1991; Xie et al., 1991). For practical applications, the latex flocculation test (Omura et al., 1984), rapid immunofilter paper assay (Cabauatan et al., 1994) and dot immunobinding assay (DIBA) (Qin, Gao & Cheng, 1994) are useful.

Relationships

RSV is the type member of the genus Tenuivirus. Serologically, it is moderately closely related to maize stripe virus (Gingery, Nault & Yamashita, 1983) and distantly related to rice grassy stunt virus (Hibino et al., 1985), but not related to rice hoja blanca virus (Yasuo, Yanagita & Yamaguchi, 1961). The amino acid sequences encoded by ORFs on RNAs 2 to 4 had a moderately high similarity to those encoded by the corresponding ORFs of maize stripe and rice hoja blanca viruses, but very low similarity to those encoded by the ORFs on RNAs 2, 5 and 6 of rice grassy stunt virus (S. Toriyama et al., 1994a, 1997, 1998). RSV has no ORF corresponding to the ORFs on RNAs 3 and 4 of RGSV. On the other hand, the amino acid sequences of the ORFs encoded on RSV RNA-1 and RGSV RNA-1 are highly conserved. The 5' and 3' termini of RSV RNAs 1-4 contain 8-nucleotide complementary sequences which are identical to those of animal viruses in the genus Phlebovirus (family Bunyaviridae) (M. Takahashi et al., 1990), and the amino acid sequence of the RSV RNA polymerase protein has appreciable homology (about 30% identity over 1500 residues) with the polymerase protein of phleboviruses (S. Toriyama et al., 1994a).

Stability in Sap

Assayed by observing transmission by injected insects. Dilution end point: 10-4-10-5 in extracts from viruliferous insects and 10-3-10-4 in sap from diseased leaves. Thermal inactivation point (5 min): 50-55 șC. Longevity: 4 days in extracts of viruliferous insects kept at 4 șC, 8-12 months in viruliferous insects and diseased rice plants kept at -20 șC, and 1-2 months in purified preparations kept at -20 șC (Kiso, Yamamoto & Kitani, 1974).

Purification

(S. Toriyama, 1982a, 1982b). Grind infected leaves in 0.1 M Na2HPO4 containing 10 mM DIECA, and adjust to pH 7.2 with solid ascorbic acid. After clarification by treatment with 20% chloroform, collect the virus by centrifugation for 2 h at 123,000g or by precipitation from 8% polyethylene glycol. Resuspend the virus in 0.01 M phosphate buffer, pH 7.5, and purify by repeated low and high speed centrifugation. Host plant impurities can be precipitated by adding solid ammonium sulphate to 30% saturation. The preparation can be further purified by centrifugation in 10-40% linear sucrose density gradients. The infective component (nB) aggregates readily and sediments to the bottom of sucrose gradient tubes: it may be necessary to resuspend the pellet and repeat the density gradient centrifugation. The yield of virus is 20-30 mg per 100g fresh leaves. Addition of Mg2+, Ca2+, EDTA or bentonite to the buffer did not improve preservation of the virus particles (S. Toriyama, unpublished data).

Properties of Particles

The virus particles sediment as three main components in sucrose density gradients: middle (M), bottom (B) and nB (Fig.4) (S. Toriyama, 1982a, 1982b). However, M component can be partially separated into two components, M1 and M2 (Ishikawa, Omura & Tsuchizaki, 1989b). A 'top component' also occurs but consists of degraded particles (S. Toriyama, 1982a).

Sedimentation coefficients (s20,w), determined on a preparation with A260=10: 72 S (M) (Koganezawa, 1977): 65 S (M), 80 S (B) and 98 S (nB) (S. Toriyama, unpublished data).

A260/A280: 1.49, determined on an unfractionated preparation (Koganezawa, Doi & Yora, 1975).

Absorbance at 260 nm (1 mg/ml, 1 cm light path): 4.4, determined on an unfractionated preparation; not corrected for light-scattering (S. Toriyama, unpublished data).

Buoyant density in caesium chloride: 1.282 g/cm3. This single component contains all the components that separate in sucrose density gradients (S.Toriyama, unpublished data).

Isoelectric point: particles precipitate at around pH 4.5 (S. Toriyama, unpublished data).

Particle Structure

The virus was formerly thought to have spherical particles (Koganezawa et al., 1975; Saito, 1977) but it is now known that the particles are basically filamentous, although they are frequently observed as apparently branched and other pleomorphic structures (Fig.5) (Koganezawa et al., 1975; S. Toriyama, 1982b). The modal length of circular filaments found in the MI, M2, B and nB centrifugal components was 510, 610, 840 and 2110 nm, respectively (Ishikawa, Omura & Hibino, 1989a). The viral structure is extremely fragile and readily unfolded. The branched appearance is caused by supercoiling: completely unfolded particles possess a helical structure 3 nm wide which in turn forms secondary coils about 8 nm wide (S. Toriyama, 1982b) (Fig.5, Fig.6, Fig.7). These unfolded pleomorphic particles folded to form stiff rod-like particles, 8 nm wide and/or circular filaments under high salt conditions (S. Toriyama et al., 1994b).

Particle Composition

Nucleic acid: ssRNA (S. Toriyama, 1982a, 1982b). However, dsRNAs containing the sequence of viral ssRNAs are also detected in agarose gel electrophoresis (S. Toriyama & Watanabe, 1989; Ishikawa et al., 1989b). The two smallest RNAs, RNA-3 and RNA-4, occur in M component (which, as mentioned above, is a mixture of two components, M1 and M2), and RNA-2 occurs in B component. The nB component contains RNAs 2 to 4 together with the largest RNA, RNA-1, and only this nB component is infectious (Fig.8) (S. Toriyama, 1982a, 1982b). The RNA constitutes about 12% of the particle weight, as judged by the A260/A280 value of purified preparations. The three RNA species from M and B components are linear molecules about 0.7-1.0 m long (S. Toriyama, 1982a).

Protein: One species of nucleocapsid protein, of 32 KDa (Koganezawa, 1977; S. Toriyama, 1982a). The sequence of 322 amino acid residues is available in the database accession numbers, D01094 and X53563 (Kakutani et al., 1991; Zhu et al., 1991). A minor, but large molecular weight protein, RNA-dependent RNA polymerase, is also associated with viral particles (S. Toriyama, 1986), and the amino acid sequence is available (database accession number D31879) (S. Toriyama et al., 1994).

Other components: No significant amounts of lipid or polyamine are found in purified preparations (S. Toriyama, unpublished data).

Genome Properties

Database accession numbers of the genome: RNA-1, D31879; RNA-2, D13176 and D13787; RNA-3, X53563, D01094 and Y11095 (China); RNA-4, D01039, D10979 and Y11096 (China). The sequences of about 20 bases at the 5'- and 3'-termini of each RNA are almost complementary to each other: ten nucleotides of these termini are identical among RNAs 1 to 4, except for one base change in RNA-1 (M. Takahashi et al., 1990).

The genome organization is shown in Fig.9. RNA-1, which encodes the RNA-dependent RNA polymerase, is negative-stranded (S. Toriyama et al., 1994a) and RNAs 2 to 4 are ambisense (Kakutani et al., 1990, 1991; Zhu et al., 1991, 1992; M. Takahashi et al., 1993). In each of RNAs 2 to 4, the intergenic non-coding region between the two ORFs contains an oligo(A)- and oligo(U)-rich sequence that can be formed into base-paired hairpin stems (Zhu et al., 1991, 1992). The nucleocapsid protein is encoded at the 5'-proximal region of virus complementary sense RNA-3, and the major non-structural protein is encoded at the 5'-proximal region of virus sense RNA-3. The major non-structural protein is synthesized in an in vitro translation system by using the viral RNA, but nucleocapsid protein is not synthesized (Hamamatsu et al., 1993). mRNAs with the genomic size of these proteins are produced in vivo, and they have an additional 10 to 23 non-viral nucleotides at the 5'-termini (Shimizu et al., 1996). At present there are no experimental data on the functions of the ORFs on viral sense RNAs 2 & 3, or on viral complementary sense RNA-4.

Relations with Cells and Tissues

Large inclusions, shaped like rings, rods or figures of eight, are present in infected cells (Kawai, 1939; Hirai et al., 1964; Reifman et al., 1978). The inclusions usually contain many granules, but some have no granules and resemble crystalline inclusions. The inclusions probably consist of the non-structural protein which is serologically unrelated to the coat protein and is produced abundantly in infected cells of plants with severe symptoms but less so or not at all in infected cells of tolerant or resistant varieties. The isoelectric point of purified non-structural protein is pH 5.4. The protein forms needle crystals at pH 4-5. Its sedimentation coefficient (s20,w) is 3 (Kiso & Yamamoto, 1973). One polypeptide species, of 20 KDa, was reported by Koganezawa (1977). The sequence of 286 amino acid residues is available in the database accession numbers D01039 and D10979 (Kakutani et al., 1990; Zhu et al., 1992).

In sections of infected plant cells (Koganezawa, 1977), recognition of individual filamentous virus particles is difficult but granular regions, sometimes enclosed by membranes, can be observed in the cytoplasm. These regions are possibly formed from virus aggregates. Virus particle antigen was detected in phloem tissue and mesophyll of infected wheat leaves by fluorescent antibody staining (Kiso et al., 1974). The virus moves downwards in the phloem at a rate of 25-30 cm/h at 30 șC and multiplies when young tissues are reached (Sonku & Sakurai, 1973a, 1973b). In viruliferous insect cells, examined by immunogold labelling of thin sections, the viral antigen was detected on amorphous or filamentous regions in the cytoplasm of the midgut, the principal salivary gland, the ovarioles and the fat body (Suzuki et al., 1992).

Ecology and Control

An epidemic of rice stripe disease in Japan was triggered by the wide introduction of the earlier cultivation of rice (Yasuo et al., 1965). It is likely that the earlier transplantation of rice seedlings coincided with the migration date of the vector L. striatellus, which had earlier multiplied in wheat fields. Thus, transplanting or seeding date affects disease incidence (Yasuo et al., 1965; Bae & Kim, 1994).

The resistance of rice (Oryza sativa) to RSV has been extensively studied. Most Japanese paddy varieties are highly susceptible but Japanese upland varieties and Indica-type rice varieties are resistant and/or tolerant. The resistance is directed against the virus, not against the insect vector. Highly resistant hybrids, Chugoku No. 31 and St No. 1, were bred by crossing cv Norin No. 8 (Japonica) and cv Modan (Indica), and then back-crossing 8 times with cv Norin No. 8. These hybrids have been used as mother lines for breeding practical new resistant varieties. Inheritance of resistance appears to be governed by multiple alleles with various levels of resistance: gene St2 in Japanese upland varieties and gene St2i in Indica-type varieties. A gene St1 at another locus as well as St2 is essential for resistance in Japanese upland varieties (Yamaguchi, Yasuo & Ishii, 1965; Sakurai & Ezuka, 1964; Washio et al., 1967, 1968a, 1968b; Sakurai. 1969; K. Toriyama, 1969, 1972; K. Toriyama et al., 1966, 1972). The cultivation of resistant varieties is favoured for decreasing the density of viruliferous insects in fields (Takayama et al., 1987).

Notes

RSV is readily distinguished from other viruses infecting rice, wheat and maize by its characteristic symptoms and by its transmissibility by L. striatellus.

The virus, together with other tenuiviruses, is evolutionarily related to phleboviruses of the family Bunyaviridae (S. Toriyama et al., 1994a). Viruses in both genera have multipartite genomes possessing negative sense and antisense components. The 5' and 3' ends of the genomic RNAs have complementary sequences of which eight nucleotides are identical in the two genera. Like viruses in most genera of Bunyaviridae, tenuiviruses infect their insect vectors as well as their primary hosts. The number of genome components and the apparent absence of a membrane-bound particle distinguish tenuiviruses from viruses in the family Bunyaviridae.

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Figure 1

Chlorotic stripe symptoms on infected leaves of rice (Oryza sativa) compared with a healthy leaf (extreme left).

Figure 2

Malformed and immature ears, and chlorotic stripes on flag-leaves, of rice plants infected at a late growth stage.

Figure 3

Drooping and wilting symptoms in young seedlings of O. sativa (cv. Norin No. 8).

Figure 4

Bands formed by rice stripe virus after sedimentation in a sucrose gradient column: middle component (M), bottom component (B) and nB component (nB).

Figure 5

Filamentous particles, c. 8 nm wide, seen in purified nB component. Bar represents 100 nm.

Figure 6

Partially and completely unfolded virus particles. Bar represents 100 nm.

Figure 7

Completely unfolded particles c. 3 nm wide. Note that they still retain a coiled appearance. Bar represents 100 nm.

Figure 8

Ribonucleic acid species on polyacrylamide gels: (left), three RNA segments from M+B components; (right), four RNA segments in a preparation from nB component, all except the uppermost being caused by contamination with M+B components.

Figure 9

Genome organization of RSV (isolate T). The ORFs of four RNA segments are displayed on viral-sense RNAs as a black bar and on viral complementary- sense RNAs as a blue bar. The proteins deduced from each ORF are shown as boxes, indicating the molecular sizes of the predicted proteins. Pol, RNA polymerase; N, nucleocapsid protein; NSmajor, a major non-structural protein.