Hibino 1996 Rice Viruses

July 10, 1996 17:9 Annual Reviews HIBINO.
TXT AR14-14
Annu. Rev. Phytopathol. 1996. 34:249–74

Copyright c 1996 by Annual Reviews Inc. All rights reserved
BIOLOGY AND EPIDEMIOLOGY

OF RICE VIRUSES
Annu. Rev. Phytopathol. 1996.34:249-274. Downloaded from arjournals.annualreviews.org
Hiroyuki Hibino
by Deutsche Forschungsgemeinschaft on 11/02/06. For personal use only.
Chugoku National Agricultural Experiment Station, Nishifukatsu 6-12-1, Fukuyama,

721 Japan
KEY WORDS: rice viruses, biology, transmission, infection cycle, epidemiology
ABSTRACT
The 15 known viruses that occur in rice are rice black-streaked dwarf, rice bunchy
stunt, rice dwarf, rice gall dwarf, rice giallume, rice grassy stunt, rice hoja blanca,
rice necrosis mosaic, rice ragged stunt, rice stripe necrosis, rice stripe, rice tran-
sitory yellowing, rice tungro bacilliform, rice tungro spherical, and rice yellow
mottle viruses. This paper describes their geographical distribution, relation to
vectors, infection cycles, field dispersal, and development, and lists recorded out-
breaks of the viruses. Many rice viruses have become serious problems since
rice cultivation has been intensified. Double-cropping of rice using improved,
photo-insensitive cultivars of short growth duration has significantly influenced
the incidence of these viruses.
INTRODUCTION
Rice, Oryza sativa L., is one of the most important cereal crops, with an annual
production of 540 m tons in an area of 150 m hectares. About 92% of the world’s
rice production comes from Asia, where the grain is consumed directly as a food
and supplies about 36% of human total calorie consumption, compared to 20%
worldwide. Rice has its origin in tropical semiaquatic grasses and is cultivated
in diverse environments: in flooded fields, uplands, deep water areas, and tidal
wetlands; in lowlands and highlands; in tropical and in temperate regions, to
53◦ N.
Of the 15 viruses known to affect rice (57, 95, 118), 12 occur in Asia, 2 in
Africa, 1 in Europe, and 1 in the American continent. In major rice-growing
countries, rice virus diseases have occurred one after another and have inflicted
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July 10, 1996 17:9 Annual Reviews HIBINO.TXT AR14-14
250 HIBINO
damage over a huge hectarage. The first major outbreak of rice viruses was
recorded in Japan in 1897 for rice dwarf virus (RDV), followed in 1903 for rice
stripe virus (RSV). From the mid-1950s to 1980s, other virus diseases have been
identified as posing serious threats to stable rice production. In many countries,
virus disease problems seem to have been accentuated by the introduction of
modern agricultural techniques, requiring intensive cultivation and resulting in
greatly increased yields (10). The rice viruses may well have been present, but
rarely reached epidemic proportions under traditional cropping when average
rice yield was low.

BIOLOGY AND EPIDEMIOLOGY

Rice Black-Streaked Dwarf Virus
Rice black-streaked dwarf virus (RBSDV) (128, 142) is a member of the fi-
jivirus group of the family Reoviridae. The virus particles are polyhedral, about
80 nm in diameter, and have 10 dsRNA segments and 5 proteins. Infected rice
plants show pronounced stunting, darkening of leaves, twisting of leaf tips,
splitting of the leaf margin, and waxy white-to-black galls along the veins on
the underside of leaf blades and the outer surface of sheaths and columns. The
galls result from hyperplasia and hypertrophy of the phloem tissues. RBSDV
is localized in the phloem and gall tissues.
RBSDV is transmitted in a persistent manner primarily by the planthop-
per, Laodelphax striatellus and two other planthopper species (57, 128). It is
propagative in the vectors but is not transmitted via eggs. In infected rice and
planthopper cells, RBSDV particles are aggregated in or around viroplasmic
inclusions or arranged in tubules in the cytoplasm of both types of cells.
RBSDV naturally infects rice, maize, wheat, barley, Alopecurus aequalis
Sobal, and some other weeds. After the rice or maize is harvested in RBSDV
endemic areas, RBSDV-infective L. striatellus moves to grass weeds and then
to barley and wheat, where it transmits the virus and oviposits (71, 90, 112,
124). The nymphs appear in September to October and overwinter as diapaus-
ing nymphs at the fourth instar. Symptoms develop on RBSDV-infected A.
aequalis, barley, and wheat plants in March, or from November to December.
Adults of the overwintered generation generally stay on the winter cereals and
oviposit. The following (first) generation acquires the virus on infected plants,
and moves to newly planted rice or maize in late May to June. It increases
greatly its number in rice but not in maize, which is not a good host of L.
striatellus. Many first-generation adults are macropterous and are capable of
flying long distances. Adults of the second and the third generations move from
the early rice to late-planted rice and disperse RBSDV. In single-cropping rice
EPIDEMIOLOGY OF RICE VIRUSES 251
areas, RBSDV incidence is generally high in early planted rice (71), whereas
in double-cropping areas, it is high in the second rice crop or late-planted rice
(124). Thus, RBSDV overwinters in L. striatellus nymphs, and also in wheat,
barley, or weeds, on which the first generation L. striatellus acquires the virus
and disperses it in rice and maize fields (71, 91, 112, 124). The incidence of
RBSDV is generally higher along the irrigation canals around rice fields (90,
119). Application of high nitrogen fertilizer results in increases of the incidence
and severity of disease (71, 90, 119).
RBSDV occurs in China, Japan, and Korea. The first major outbreaks of
RBSDV in Japan was recorded in maize in the years 1957–1961, and in rice
and maize in 1965–1967. In China, an outbreak occurred in 1963 and in 1965–

1967 in rice, maize, wheat, and barley. The incidence of RBSDV was high
in 1975–1976 in Korea (90). Except for these periods of high incidence, the
occurrence of RBSDV was local, and the incidence was generally low in all
three countries. RBSDV frequently caused severe damage in maize but lesser
damage in rice, or vice versa, in the same locations. In Tohoku, in northern
Japan, RBSDV affects maize but not rice. In one locality in Hokkaido, north
of Tohoku, it occurs in rice, although the incidence is low.
The high RBSDV incidence in Japan coincides with the period when the
area planted for early rice increased. The decreased incidence after 1968 is due
largely to a decline in the area planted for wheat and barley. The outbreak in
1963 to 1967 in China was attributed to increased wheat cultivation (143). The
decrease in the incidence in China after 1970 was attributed to the promotion
of double and triple cropping of rice, which resulted in a reduction of areas
planted for wheat. That the major outbreaks of RBSDV occurred at about the
same time in Japan and China indicates a possible correlation between them.
The vector L. striatellus migrates from southern China to Japan and may also
move in the opposite direction, although the annual migration is limited (85).
Rice Bunchy Stunt Virus
Rice bunchy stunt virus (RBSV) (93, 146) is a possible member of the phy-
toreovirus group. The virus particles are polyhedral, about 60 nm in diameter,
and have 12 segments of dsRNA. Infected rice plants show stunting, increased
tillering, and short and/or narrow leaves.
RBSV is transmitted in a persistent manner by Nephotettix cincticeps and
N. virescens (16, 146). It is propagative in the vectors but is not transmitted
via eggs.
Rice is the only known host of RBSV. In Fujian, China (144, 149), N. cinc-
ticeps and N. virescens that acquire RBSV on late-planted rice plants stay on
ratooned rice or on grass weeds, overwinter at the nymph or adult stages, and dis-
perse the virus to nursery beds or newly planted rice fields in early spring (149).
252 HIBINO
Some RBSV-infected ratoons also overwinter and develop new leaves that serve
as a virus source for the early planted rice. The incidence of RBSV is generally
higher in the second crop rice, and is also higher at the edges of fields (144).
RBSV has been reported in Fujian, Gaundong, Guanxi, Hubei, Hunan,
Jiangxi, Queichou, and Yunnan in China (148). A survey during 1976–1981
found that the incidence in these locations was generally low and often nil.
Average incidence was higher in 1979 than in other years.
Rice Dwarf Virus

Rice dwarf virus (RDV) (66, 142) is a member of phytoreovirus group of
the family Reoviridae. The virus particles are polyhedral, about 70 nm in

diameter, and have 12 segments of dsRNA and 7 proteins, one of which is
serologically cross-reactive with the corresponding protein of rice gall dwarf
virus. Infected rice plants show pronounced stunting, increased tillering, and
short leaves that are darker green in color and with fine chlorotic specks. RDV
is distributed in vascular bundles and in parenchymatous cells in the portions of
leaves that correspond to the white specks. Infected cells contain large round
or oval inclusion bodies in the cytoplasm. The bodies consist of a viroplasmic
matrix and numerous virus particles. Tubules enclosing virus particles and
paracrystalline bodies occur in or around the bodies (H Hibino, unpublished
observation). Starch accumulates in infected rice tissues.
RDV is transmitted in a persistent manner by Nephotettix cincticeps, N. ni-
gropictus, Recilia dorsalis, and some other Nephotettix spp. (57, 66). N.
cincticeps is the most significant vector. RDV is propagative in the vectors
and transmitted from female adults to their progeny via eggs. RDV-infected N.
cincticeps has lower fecundity, higher nymphal mortality, and shorter longevity
(105, 109). The vector ability of populations of N. cincticeps varied location-
ally. In infected vector cells, RDV particles occur in or around viroplasmic
inclusions, in phagocytic vesicles, or in tubules in the cytoplasm. Virus parti-
cles occur in mycetocytes in close association with symbiotic organisms that
are transmitted via eggs (110).
RDV naturally infects rice and a few grass weeds. The weed hosts are
probably not important reservoirs of the virus (70, 129). After the late-planted
rice is harvested, infective N. cincticeps move to grass weeds and overwinter as
nymphal diapauses (67, 70, 82, 91, 106). Adults of the overwintered generation
appear in March or April, and stay generally on weeds. In warm areas where
rice is planted in early April or May, some leafhoppers move to rice and spread
the virus. The first-generation adults, which are congenitally infected with
RDV, appear in June and move to newly planted rice fields.
The population of N. cincticeps decreases during the winter season, remains
at a low level in the first generation, and increases rapidly after it moves into
rice fields. The percentage of infective N. cincticeps in the populations is high

in areas where RDV incidence is high. The percentage also changes depending
on cropping patterns and seasons. It is higher in the first than subsequent
generations in areas where rice is planted early, but it is lower in the first and
second generation in areas of medium and late rice (106). These changes were
attributable to lower fecundity and shorter life span of RDV-infected females,
especially at high temperature (105, 109).
In rice double-cropping areas in China, the second- and the third-generation
adults, which are infective, disperse RDV from the first- to second-crop rice
(20, 21, 91). The incidence of RDV is generally higher in the second than
in the first crop. The incidence in the second-crop rice is correlated with the
percentage of RDV carriers in the overwintering generation (91), and with the
percentage and density of RDV carriers in the second generation (17). The
population of N. cincticeps declines to a low level during the winter season and
increases from generation to generation after the start of the rice season (91).
RDV incidence is generally higher at the edge of fields. Application of
excess nitrogen fertilizer results in an increase of the vector population and the
susceptibility of rice plants to RDV, with a consequent increase in incidence of
the virus (71). Epidemiological models of RDV have been developed in Japan
(102, 104) and models for second-crop rice in China (17, 144).
RDV occurs in China, Japan, Korea, and Nepal, and was recently reported
in Mindanao, the Philippines (12). In southern and central Japan, high local
incidence of RDV was recorded from time to time during the period 1889–1930.
After 1955, however, the incidence of RDV reached epidemic proportions first
in southern Japan, then in central Japan (81). The incidence was especially high
from 1967 to 1978 and declined thereafter. In Chejiang, China, the incidence
was high from 1969–1973 (91). The epidemic in Japan that started around 1955
was correlated with the increase in areas planted for early rice, which allowed the
first generation of N. cincticeps to multiply and to disperse the virus in rice, and
which raised vector density and the proportion of vectors that were infected with
the virus. The spread of the epidemic even farther after 1967 was attributable to
several interconnecting factors: Cropping of winter wheat and barley in paddy
fields decreased steadily after 1955; this in turn increased the number of rice
fields left fallow during the winter season and favored the overwintering of N.
cincticeps on weeds; meanwhile, vector populations developed resistance to
pesticide (81, 107). The decreased incidence of RDV after 1979 was attributed
to the application of insecticide to rice seedlings in nursery boxes for machine
transplanters and to the plowing of fallow rice fields in winter or early spring.
254 HIBINO
Rice Gall Dwarf Virus

Rice gall dwarf virus (RGDV) is a member of phytoreovirus group of the
family Reoviridae (115, 142). The virus particles are polyhedral, about 65 nm
in diameter, and have 12 segments of dsRNA and 7 proteins, one of which is
serologically cross-reactive with the corresponding protein of RDV. Infected
rice plants show pronounced stunting, a reduced number of tillers, short darker
green leaves, and small galls along the leaf veins on the under surface of leaves
and the outer surface of sheaths. The galls result from hyperplasia and hy-
pertrophy of the phloem tissues. In infected plants, RGDV is localized in the

phloem and gall tissues. In infected plant cells, RGDV particles are aggregated
or scattered in or around viroplasmic inclusions, or arranged in tubules in the

cytoplasm.
RGDV is transmitted in a persistent manner by N. cincticeps, N. nigropictus,
Recilia dorsalis, and some other Nephotettix spp. (57, 115). RGDV is prop-
agative in the vectors and is transmitted from female adults to their progeny
via eggs. In infected N. cincticeps cells, virus particles are packed in phago-
cytic vesicles, or scattered in association with bundles of microfilaments or in
viroplasmic matrix in the cytoplasm.
RGDV naturally infects rice and the grass weed Alopecurus aequalis (150).
In southern China, RGDV-infected ratoons and volunteer rice plants over-
winter and provide a reservoir of virus inoculum in the spring (150). Also,
RGDV-infected A. aequalis and leafhopper vectors overwinter and serve as
virus sources. The percentage of RGDV-infective leafhoppers in overwintered
populations is higher for R. dorsalis than for other vectors.
RGDV occurs in Fujian and Guandong, China (148), in Malaysia, and
in Thailand (115). An outbreak of RGDV occurred in the western part of
Guandong in 1981–1982 (150). The areas affected reached 7000 ha in 1981
and 33,000 ha in 1982, and the yield loss was estimated at 2400 kg/ha in mod-
erately affected fields and 4500 kg/ha in severe cases. RGDV incidence has
been low since 1983. In Thailand, RGDV is generally sporadic and causes only
incidental reduction in yields.
Rice Giallume Virus

Rice giallume virus (RGV) is a strain of barley yellow dwarf luteovirus (9,
116). The virus particles are polyhedral, about 25–28 nm in diameter, and
have a single molecule of ssRNA and a single protein. RGV-infected rice
plants show stunting, reduced tillering, and yellow-to-orange discoloration of
leaves. Infected plants may die prematurely. In infected rice plants, RGV
particles are localized in the phloem tissues. In infected rice cells, virus particles
are scattered or aggregated in the cytoplasm. Infected cells contain double-
membraned vesicles with fibrils, degenerated mitochondria, and deposits of

opaque materials along the cell wall.
RGV is transmitted in a persistent manner by Rhopalosiphum padi and some
other aphids (116). RGV is likely nonpropagative, but is circulative in the
vectors.
RGV naturally infects rice and some cereals and grass weeds, including
Leersia orizoides (L) Sw (1, 2, 117), which is a common perennial grass in and
around rice fields and which also serves as a host of R. padi in the absence of
rice. RGV overwinters in L. orizoides. In rice fields, L. orizoides develops new

leaves before rice seedlings start to grow and attracts R. padi (117). Giallume-
diseased plants often appear in patches in the fields. These foci of infected
plants are associated with RGV-infected L. orizoides in the fields.
Barley yellow dwarf virus is distributed worldwide, but infection of rice by
strains of the virus has not been reported outside of northern Italy and Spain
(116).
Rice Grassy Stunt Virus
Rice grassy stunt virus (RGSV) is a member of the tenuivirus group (56, 139).
The virus particles are circular filaments, 6–8 nm in width, with possibly four
ssRNA molecules with plus and minus polarities, and coat protein and RNA
polymerase. RGSV is serologically distantly related to RSV. RGSV-infected
rice plants show pronounced stunting and proliferation of short, erect, and nar-
row leaves that are pale green or pale yellow in color. Infected leaves may show
mottling symptoms. RGSV strains that cause yellow-orange leaf discoloration
and premature death of plants were detected in 1977 in Taiwan (13), in 1982–
1983 in the Philippines and Thailand (59), and in 1984 in India (100). The
severe strain that occurred in Taiwan was called rice wilted stunt virus. RGSV-
infected plants produce a virus-specific protein that is serologically related to a
similar protein produced in RSV-infected plants. RGSV-infected rice cells con-
tain masses of fibrils in the nuclei and cytoplasm and membrane-bound bodies
with fibrils in the cytoplasm. Tubules associated with isometric particles, 18 to
25 nm in diameter, can be seen in the sieve tubes.
RGSV is transmitted in a persistent manner by the brown planthopper Nila-
parvata lugens and by two other Nilaparvata spp. (56, 57). It is propagative in
the vectors but is not transmitted via eggs. N. lugens, one of the most important
pests of rice in Asia, causes feeding damage or “hopper barn.” Average lifespan
and fecundity are lower in RGSV-infective than in virus-free N. lugens (64, 96).
Populations of N. lugens in which RGSV-transmission ability is low can be se-
lected by mating noninfective hoppers (73). Isometric particles similar to those
found in infected rice tissues are found in crystalline arrays in the fat body and
tracheas of infected N. lugens.
256 HIBINO
RGSV naturally infects only rice. The vector N. lugens is monophagous

to rice. It flies from grassy stunt–affected fields to newly planted rice fields in
distant areas and disperses RGSV and another N. lugens-borne virus, rice ragged
stunt virus. In the tropics, RGSV and N. lugens are generally endemic in areas
where rice is planted year-round. In cooler areas where rice is not planted during
the winter season, N. lugens migrates annually during the monsoon season from
the endemic areas (19, 84, 89, 108). Some of the migrant planthoppers, which
travel enormous distances over sea, carry RGSV (63, 74). Infected rice stubble
and volunteer rice plants also serve as a source of the virus. When the incidence
of RGSV is high, the rice crop also suffers direct damage from feeding by N.
lugens, and in addition from rice ragged stunt virus.

Rice cultivars with resistance to N. lugens have been planted widely in Asia.
Incidence of RGSV is low to nonexistent in these resistant cultivars. However,
populations of N. lugens (biotypes) that can overcome the resistance have devel-
oped a few or several years after release of the cultivars (26). Once populations
of N. lugens developed that could feed and colonize in cultivars possessing a
resistance gene, the cultivars showed no more resistance to RGSV in the fields
and became subject to severe grassy stunt. In the Asian tropics, there had been
widespread use of rice cultivars with a resistance gene to RGSV introduced from
a line of the wild rice, Oryza nivara (80). The severe strain of RGSV (RGSV-2)
that occurred in the Philippines was highly pathogenic to the resistant cultivars
(59).
RGSV occurs in south and southeastern Asia, China, Japan, and Taiwan.
RGSV incidence was high from 1970–1977 in Indonesia; from 1973–1977
and in 1982–1983 in the Philippines (57, 59); in 1973–1974 and in 1981 in
Kerala, India (88); in 1972 and 1984 in Tamil Nadu, India (100); and in 1978
in Kyushu, Japan (75). Since 1984, the incidence of RGSV has been generally
low in Asia. Although not well documented, the low incidence is thought to
be due to a change in virus transmission ability of N. lugens populations. In
the Philippines, the proportion of RGSV transmitters in populations that have
fed on RGSV source plants ranged from 3 to 50% before 1977 (96), but from
0–15% in 1984 (64; H Hibino, unpublished observation).
Rice Hoja Blanca Virus
Rice hoja blanca virus (RHBV) is a member of the tenuivirus group (103).
The virus particles are filamentous, 3 nm in width, and have possibly four
ssRNA strands of plus and minus polarities and coat protein. RHBV-infected
rice plants show stunting, chlorotic or yellow striping and mottling of leaves,
and premature wilting. Rice cells infected with RHBV contain large masses
of fine filaments, 8–10 nm in width, in the nuclei and cytoplasm. Infected
plants produce a large amount of virus-specific proteins. RHBV is serologically
related to Echynochloa hoja blanca virus species but not to other members of the
tenuivirus group. The virus-specific protein of RHBV is serologically related

to the similar protein in Echynochloa hoja blanca virus–infected plants.
RHBV is transmitted in a persistent manner by Sogatodes orizicola (Muir)
(103). Sogatodes cubanus is capable of transmitting the virus from rice to
their grass hosts but not from rice to rice, which is not a host of S. cubanus
(31, 45). RHBV is propagative in the vectors and is transmitted at a high
rate from female adults to their progeny via eggs. The percentage of infective
planthoppers in colonies can be increased to 90–100% by selective breeding
(46, 51). S. orizicola with newly acquired RHBV becomes infective after an
incubation period of 30–36 days (44). Because of the long incubation period
of the virus in S. orizicola, planthoppers that acquire RHBV through feeding

on infected plants rarely live long enough to transmit the virus. S. orizicola
infected with RHBV have a shortened life span, low fecundity, and reduced
nymph viability (29, 76).
RHBV naturally infects only rice. S. orizicola colonizes only on rice and
a few wild rice species (27). RHBV is dispersed primarily by S. orizicola
congenitally infective of the virus.
RHBV occurs in Central and South America, in the Caribbean, and from
1957–1959 in the southern United States (5). The first outbreak of RHBV
occurred in Latin America during the years 1956–1967. From 1965–1967,
however, damage caused by the vector, S. orizicola, was more severe than that
caused by the virus (76). The disease did not cause any serious economic
problems from 1968–1980, but when it reappeared in some Latin American
countries from 1981–1985, it reached epidemic proportions (152). S. orizicola
was observed in 1957, 1959, and 1962 in rice growing areas of the southern
United States (5).
In Latin American countries, rice hoja blanca, which occurred only sporadi-
cally before 1957 (4), became important after the introduction and widespread
cultivation of new rice cultivars. There was a very large increase in sogata den-
sity in western Cuba and Venezuela after the introduction of short-maturing rice
varieties that made multiple cropping possible (31). The cyclic nature of the hoja
blanca epidemic is explained by the deleterious effects of RHBV on S. orizicola
and the possible selection of virus noninfective populations (152). The plant-
hopper’s ability to support replication of the virus is inherited, and susceptibility
to the virus in wild populations may be lowered after the outbreak of disease.
Rice Necrosis Mosaic Virus
Rice necrosis mosaic virus (RNMV) is a member of the bymovirus group of the
family Potyviridae (40, 69). The virus particles are flexuous filaments, 205 and
550 nm in length and 13–14 nm in width, and contain 2 ssRNA strands and a sin-
gle protein. The virus is serologically related to barley yellow mosaic and wheat
yellow mosaic viruses. RNMV-infected rice plants show moderate stunting;
258 HIBINO
reduced number of tillers; a spreading growth habit; elongated or spindle-

shaped, yellow flecks and streaks on the lower leaves; and necrotic flecks at
the basal portions of stems and sheaths. In infected rice cells, RNMV parti-
cles are scattered or associate with laminated aggregates and pinwheels in the
cytoplasm. Infected cells have complex membranous bodies in the cytoplasm.
RNMV is transmitted by the soilborne fungus Polymyxa graminis (40).
Zoospores from zoosporangia or resting spores of P. graminis that develop
in RNMV-infected root cells penetrate into the root cells of other plants and
transmit the virus. Two isolates of the virus, one from Japan and one found
at Cuttack, India, which are thought to be RNMV, were transmitted to rice by
mechanical means (42, 47), but mechanical transmission of other RNMV iso-
lates proved difficult (40). The Japanese isolate was transmitted from infected
plants to the next generation through seeds (41), but no seed transmission of
the virus has been reported for other isolates (40). The two isolates have not
been well characterized.
RNMV-affected soil (i.e. containing P. graminis) retains infectivity for many
years (40). RNMV infection of rice seedlings through soil is high when the soil
reaches a temperature of 25–30◦ C and soil moisture is low. Because wet soil is
not favorable for infection, RNMV is rare in rice seeded directly into flooded
fields. Rice necrosis mosaic occurred either in transplanted fields or in fields
seeded directly and grown under an upland condition. In transplanted fields,
rice necrosis mosaic occurs only when seedlings are infected with RNMV in
nurseries. Plant infection with RNMV after transplanting is rare. In Japan, after
the introduction of machine transplanters using seedlings prepared in nursery
boxes, the incidence of RNMV declined rapidly and disappeared in most af-
fected areas. Many upland rice cultivars in Japan have a high level of resistance
to the disease, and the incidence of RNMV is generally low in upland rice fields
(40).
Rice necrosis mosaic was first recognized in 1959 in Okayama, Japan, and
subsequently during 1962–1970 in southwestern and central Japan (40). A
similar disease occurred once only in Cuttack, India (47). All isolates of RNMV
except the Indian isolate only infect rice naturally. The Indian isolate naturally
infects weeds, Ludwigia perennis and Brachiaria ramosa (48). Infected L.
perennis show increases in height, leaf size, and stem diameter (49). The role
of these weeds in the disease cycle is not known.
Rice Ragged Stunt Virus
Rice ragged stunt virus (RRSV) is a member of the oryzavirus group of the
family Reoviridae (101, 142). The virus particles are polyhedral, about 50 nm
in diameter, and contain 10 dsRNA strands and 5 major proteins. Infected rice
plants show stunting, abnormal leaves with serrated edges or twisted tips, and
vein swelling or galls on the underside of leaf blades and outer surface of the
leaf sheaths. The gall results from hyperplasia and hypertrophy of the phloem
tissue. Plants infected with RRSV at the seedling stage develop new leaves
with identifiable symptoms two weeks after inoculation and thereafter develop
leaves showing milder or no definite symptoms. At the heading stage, the plants
again show symptoms on upper leaves and flag leaves. In infected plants, RRSV
is localized in the phloem and gall tissues. Infected cells contain large inclusion
bodies consisting of a viroplasmic matrix and numerous virus particles.
RRSV is transmitted in a persistent manner by the brown planthopper, Nila-

parvata lugens, and another Nilaparvata spp. (57, 101). It is propagative in the
vectors but is not transmitted via eggs. In infected vector cells, RRSV particles
are aggregated in or around the viroplasmic inclusions or arranged in tubules
in the cytoplasm.
RRSV infects many graminaceous plants in inoculation tests using N. lugens.
Natural infection of weeds and cereals other than rice is rare or nonexistent,
as N. lugens is monophagous to rice (53, 101). In the Asian tropics, RRSV
and the brown planthopper are endemic in irrigated areas where rice is grown
throughout the year. RRSV-infected planthoppers are the primary source of the
virus. Macropterous adults of N. lugens move from RRSV-damaged fields to
newly planted rice fields and spread the virus.
As described for rice grassy stunt virus, rice cultivars possessing resistance
genes to N. lugens have been planted widely in Asia. Resistant cultivars that
formerly had little or no ragged stunt had severe infestations when populations
of N. lugens developed that were able to feed and colonize in these cultivars.
The occurrence of rice ragged stunt was first recognized in 1977 in Indonesia,
Malaysia, the Philippines, and Thailand; in 1978, in China, India, Sri Lanka
(53), and Taiwan (14); and in 1979, in Japan (131). The origin of RRSV is
not known. In many of these countries, RRSV soon reached epidemic levels:
incidence was high in 1977–1981 in Indonesia and the Philippines, and in 1980–
1982 and 1989–1990 in Thailand. Incidence has generally been low in many
countries since 1982, except in Thailand and Vietnam. RRSV may have long
been present at a low level in many of these countries (97). In the Asian tropics,
however, the population density of the vector N. lugens increased dramatically,
and another N. lugens–borne RGSV reached epidemic proportions in many
countries in the 1970s (30). That RRSV was present but unnoticed for many
years is unlikely given the severity of infestation with the vector (97). RRSV
may have been localized in an area where the vector population was relatively
low in the early 1970s. Since N. lugens is capable of long-distance transoceanic
flight (84), RRSV might have been dispersed during 1977–1979 from localized
areas to other areas through long-distance flights by N. lugens.
260 HIBINO
Rice Stripe Necrosis Virus

Rice stripe necrosis virus RSNV is a possible member of the furovirus group
(36, 37). The virus particles are rod shaped, 120, 270, or 380 nm in length and 20
nm in width. RSNV naturally infects only rice. Infected plants show stunting,
reduced number of tillers, and chlorotic or yellow stripes on leaves, which later
become necrotic. In RSNV-infected cells, virus particles are aggregated in the
cytoplasm. Paracrystalline inclusions occur in the cytoplasm of infected cells.
RSNV is soilborne and is maybe transmitted by the fungus Polymyxa grami-
nis. However, it is also mechanically transmissible.

Rice stripe necrosis was first reported in the Ivory Coast in 1977 (99). The
disease occurs in the Ivory Coast, Liberia, Nigeria, and Sierra Leone (37). In
disease-affected fields, stripe necrosis occurs erratically from season to season.
Disease incidence in upland rice is higher when short periods of intermittent
rain are interspersed with long dry periods at the beginning of the rainy season.
In the fields, the disease appears in patches, which expand progressively.
Rice Stripe Virus

Rice stripe virus (RSV) is the type member of the tenuivirus group (138, 139).
The virus particles are circular filaments 290, 510, 610, 840, or 2110 nm in
length and 9 nm in width. Virus particles contain five strands of ssRNA of
plus and minus polarities, coat protein, and RNA polymerase. RSV is sero-
logically related to maize stripe virus and RGSV. Infected rice plants show
chlorotic stripes or mottling and necrotic streaks on leaves, and premature wilt-
ing. Chlorotic leaves are unfolded, and later droop and wilt. Infected plants
produce relatively high concentrations of virus-specific proteins, which are
serologically related to similar protein produced in RGSV-infected plants. In-
fected rice cells contain large masses of granular or sandy structures in the
cytoplasm and nuclei and masses of needlelike and paracrystalline structures
in the cytoplasm and vacuole.
RSV is transmitted in a persistent manner by Laodelphax striatellus and
some other planthoppers (57, 138). It is propagative in the vectors and trans-
mitted from female adults to their progeny via eggs. The effects of RSV on L.
striatellus are uncertain. Nasu (109) reported lower fecundity, higher nymphal
mortality, and shorter life span in L. striatellus that have been infected with RSV.
Kishimoto (86) found no such adverse effects on the planthopper. The vector
ability of L. striatellus is controlled genetically (83). Populations of L. striatel-
lus with low or high virus transmission (acquisition) ability can be obtained by
selective breeding (83). RSV is mechanically transmissible, but with difficulty.
RSV naturally infects rice, wheat, barley, oat, foxtail millet, and some gram-
inaceous weeds (138). These cereals, with the exception of rice and winter
weeds, are not good hosts of RSV and do not serve as virus sources for the next
crop season. After rice is harvested from September to October in central and
southern Japan, infective L. striatellus moves to grass weeds and then to wheat
and barley where it transmits the virus and oviposits (23–25, 113, 141, 151).
Nymphs appear in late September to October and overwinter as diapausing
nymphs on wheat, barley, and grasses. In March, adults of the overwintered
generation appear, and some may move to early rice. The following (first) gen-
eration is congenitally infective and prolific. From the end of May to mid-June,
the first-generation adults, many of which are macropterous, move to newly
planted rice fields and transmit the virus. The major infection of rice is incurred
by the first-generation adults and the second-generation nymphs. Generally,
virus incidence is low in rice fields planted very early in April, high in fields
planted in May, and lower again in fields planted later. Rice plants infected with
the virus at the early growth stage show severe symptoms and die prematurely.
Plants exposed to infective L. striatellus at later growth stages had less infection
and showed milder symptoms and no wilting. In northern Japan (Hokkaido),
RSV-infected adults of the overwintered generation appear from May to June,
move to newly planted rice seedlings, and transmit the virus (78). In Japan, the
incidence of RSV in the following crop season can be estimated by the density
and percentage of RSV carriers in the overwintering populations (86).
RSV occurs in China, Japan, Korea, Siberia, and Taiwan. In Japan, the
incidence of RSV was very high from 1960–1972 and increased again from
1977–1986 (81). In Korea, it was high during 1964–1965 and 1973–1974
(23). In China, high incidence was recorded in 1964 in Shanghai and Jiangso,
Zhejiang; in 1975–1976 in Beijing; in 1984 in Shandong; and repeatedly from
1974–1990 in Yunnan (94). The increase during the 1960s in Japan was due
largely (1) to an increase in the areas planted to early maturing rice, which
provides favorable conditions for L. striatellus and RSV, (2) to increased winter
wheat and barley production, which supports a large planthopper population
during the winter season, and (3) to staggered planting of early to late rice,
which serves as a continuous source of virus-susceptible young seedlings (81).
The decrease in incidence after 1973 was due to the decline in areas planted
for winter wheat and barley that had started around 1960. In the late 1970s,
the areas increased to some extent. The second epidemic in Japan started in
1977 when L. striatellus populations were very high in Kanto (central Japan). In
areas where RSV was epidemic, rice cultivars resistant to RSV were introduced
in 1981, and as areas planted for the cultivars increased (111, 134), incidence
declined to a low level in Kanto by 1988. RSV is endemic in localized areas in
central and western Japan.
Rice Transitory Yellowing Virus
Rice transitory yellowing virus (RTYV) is a member of the subgroup nucle-
orhabdovirus of the plant rhabdovirus group (127). It is identical or very close
262 HIBINO
to rice yellow stunt virus, which was identified at about the same time in China
(35). Virus particles are bullet shaped, 180–210 nm in length, and 94 nm in
width, and have ssRNA and 4 or 5 proteins. Rice plants infected with RTYV
show leaf yellowing, reduced tillering, and mild stunting. Later, infected plants
develop normal-looking leaves and may appear healthy, but symptoms may
reappear after this temporary recovery. In infected rice plants, RTYV is local-
ized in the phloem tissues. A mass of RTYV particles appears between two
nuclear membranes in infected cells.
RTYV is transmitted in a persistent manner by Nephotettix cincticeps, N.

nigropictus, and N. virescens (57, 127). It is propagative in the vectors but
is not transmitted via eggs. Vector efficiency is high in N. cincticeps and

N. nigropictus, but low in N. virescens. In infected leafhopper cells, RTYV
particles are found in vacuolate structures in the cytoplasm.
RTYV naturally infects only rice. After the harvest of late-planted rice,
RTYV overwinters in rice stubble or in the vector, N. cincticeps. N. nicropictus
lives on weeds, and its density is generally low in rice. N. nigropictus and
weed hosts may play a role in the infection cycle of RTYV in hillside areas.
Overwintering hosts of the virus are rice stubble in southern China (33), in N.
cincticeps and occasionally in rice stubble in Fujian, China, and Taiwan (15,
142), and in N. cincticeps in the middle and lower basin of the Yangtze River,
where rice stubble is unable to overwinter (18, 91). After early planted rice
is harvested, second- or third-generation adults of N. cincticeps move to the
late-planted rice and spread the disease.
The incidence of RTYV is generally low in the first rice crop and high in
the second crop (15, 17). Under epidemic conditions, the incidence of RTYV
in the second crop is correlated to the rate of RTYV-infective N. cincticeps in
the population, N. cincticeps density, and winter temperatures (15, 17, 18, 92)
and to virus incidence in early rice and the rate of infective leafhoppers in the
population in June (145). RTYV and RDV, which have common vectors, N.
cincticeps and N. nigropictus, frequently occur together in southern and central
China (17, 91, 145).
RTYV occurs in southern and central China, the Nansei Islands (Okinawa)
of Japan, Taiwan, and Thailand (57). Rice yellow stunt virus has been reported
in Vietnam (140) and Laos (126). Major outbreaks of RTYV occurred in 1960–
1962, 1973–1975, and 1977–1980 in Taiwan (15, 22, 133); in 1964–1966 and
in 1979 in Guandong, China (33); in 1966, 1969, and 1973 in Fujian (145);
and in 1970–1972 in Cheijang (18). The incidence has generally been low
since the mid-1980s. In 1979, RTYV was found in Chiengrai and Chienmai,
Thailand (68). Areas affected were localized, and its incidence is generally low
in Thailand.
Rice Tungro Bacilliform and Rice Tungro Spherical Viruses

Tungro (4, 58) is the most important virus disease of rice in the Asian tropics. It
is a composite disease caused by rice tungro bacilliform virus (RTBV) and rice
tungro spherical virus (RTSV). RTBV is a member of the badnavirus group.
Virus particles are bacilliform, 100–300 nm in length and 30–35 nm in width.
RTBV has a circular dsDNA and a single protein. RTSV is a member of the
ribotungrovirus group. Virus particles are polyhedral, about 30 nm in diameter.
RTSV has ssRNA and three proteins.
Rice plants infected with RTBV and RTSV together show tungro symptoms,
including stunting, yellow or yellow-orange discoloration, and reduced tillering
(61). Discolored leaves may show irregularly shaped dark-brown blotches.

The leaves, especially the younger ones, may show striping or mottling and
intervernal chlorosis. Plants infected with RTBV alone show similar but milder
tungro symptoms. Plants infected with RTSV alone show no obvious symptoms
except very mild stunting. In infected plants, RTBV is localized in the vascular
bundles and RTSV in the phloem tissues (132). In infected cells, both RTBV and
RTSV particles are scattered or aggregated in the cytoplasm. RTSV particles
also occur in vacuoles. Viroplasm-like inclusions and membraneous masses
occur in the cytoplasm of RTSV-infected cells.
RTBV and RTSV are transmitted in a semipersistent manner by Nephotet-
tix virescens, N. nigropictus, N. cincticeps, Recilia dorsalis, and some other
Nephotettix spp. N. virescens is the most efficient vector of tungro disease (54,
62, 79). N. cincticeps is the principal vector of rice waika virus (RTSV) in Japan
and probably serves as the vector of tungro in southern China. N. nigropictus
and R. dorsalis are less efficient vectors of RTBV and RTSV. Immediately after
feeding on source plants infected with RTBV and RTSV, the vector leafhopper
transmits the viruses, either both viruses together or RTBV or RTSV alone. It
retains RTBV for 4–5 days and RTSV for 2–4 days. The leafhopper readily ac-
quires RTSV on source plants infected with RTSV alone, but it does not acquire
RTBV on plants infected with RTBV alone (61). Leafhoppers that have fed
previously on RTSV-infected plants acquire RTBV from plants infected with
RTBV. Through feeding on plants infected with RTBV, the leafhopper gains a
helper component and thus the ability to acquire RTBV. The leafhopper retains
the helper activity for the acquisition of RTBV for seven days. After feeding
on antiserum to RTSV, the leafhopper loses RTSV infectivity but retains the
helper activity (60). After molting, leafhoppers lose both RTBV and RTSV
infectivity (67, 95), as well as the helper activity (11). RTSV is unlikely to be
a bearer of the helper activity. The helper component may be a protein coded
on the RTSV genome and produced in RTSV-infected cells, similar to those for
potyviruses and caulimoviruses (120). Both RTBV and RTSV are stylet-borne,
264 HIBINO
and the helper component may be essential for specific adsorption of RTBV on
the leafhopper’s mouth wall. The helper component has not been isolated from
plants infected with RTSV. The helper gene has not been located on the RTSV
genome.
N. virescens is monophagous to rice, and its density can reach high levels de-
pending on the environment. After rice is harvested, the density of N. virescens
falls rapidly to a low level or to nil in the rice fields. Rice is likely the only host
of RTBV and RTSV, although all wild rice tested thus far and perhaps some
weeds also can be infected with RTBV and/or RTSV by exposing to RTBV
+ RTSV or RTSV-infective N. virescens (3, 79, 87). Tungro-infected plants
including rice stubble or volunteer rice serve as sources of RTBV and RTSV.
N. virescens that feeds on source plants moves to newly transplanted fields in
surrounding areas (136) and disperses the viruses. Although the flying ability
of N. virescens is not known, its range is suspected to be several kilometers or
more. In Kyushu, Japan, rice stubble infected with rice waika virus overwinters
and develops new leaves in spring, which serve as the source of the virus (72).
Tungro-infective N. virescens lands on newly planted rice fields, transmits
the viruses to one or more rice seedlings, which then serve as the source for
further dispersal in the field. Generally, plants with secondary infection from
such sources form patches a few to several meters in diameter, which later fuse
with each other. Generally, in tungro-endemic areas, major infection of rice
plants with RTBV and RTSV occurs after transplanting, and the infection rate
in seedbeds prepared in the field is low (137). In transplanted fields, infection
with RTSV alone precedes infection with RTBV (137), as the source of RTSV
is more prevalent in surrounding fields (6). RTSV is often spread alone as an
independent but a latent disease (6).
Tungro incidence is generally low in fields planted in the early crop season
when the vector population is low, but it is high in fields planted later when the
vector population is higher (125). Tungro incidence is not necessarily correlated
to vector density (4, 98), although vector density is much higher in epidemic
than in nonepidemic years.
In the Asian tropics, rice cultivars possessing resistance to N. virescens have
been used widely to control tungro disease (58). Many resistant cultivars that
formerly had a little or no tungro sustained severe damage several years after
the release of the resistant cultivars because of the development of populations
of N. virescens able to feed and colonize on the cultivars (28, 58).
The practice of definite fallow periods after each crop season in each area
has been followed in Indonesia and Malaysia to solve the tungro problems.
In South Sulawesi, Indonesia, an integrated tungro management scheme has
been successfully practiced since 1983 (125). In this scheme, rice planting was
scheduled to have nearly synchronous growth and to maintain a definite fallow

period after the harvest of each crop in each area, in addition to the deploy-
ment (rotation) of cultivars with different resistance to N. virescens. Under the
scheme, tungro incidence was zero or negligible when planting occurred on
schedule or up to one month later, but it was high when planting occurred two
or three months later. Low tungro incidence under the management scheme
was mainly attributable to the slow rate of increase in the vector population and
to the absence or paucity of sources of tungro in the area.
Tungro disease occurs in south and southeastern Asia and in southern China
(57, 147). RTSV alone (rice waika virus) was once epidemic in Kyushu, Japan
(43, 130). The occurrence of RTSV alone has been reported in Shandong, Fubei,
Funan, Fujian, Jiangxi, Guandong, and Hainan in China (148). Major outbreaks
of tungro occurred in 1969 in Bangladesh; in 1969, 1984, and 1985 in India;
from 1969–1971, 1972–1975, 1980, 1984–1985, and 1994–1995 in Indonesia;
in 1969 and 1982–1983 in Malaysia; in 1957, 1970–1971, and 1983–1984 in the
Philippines; and from 1965 to 1970 in Thailand (57). As indicated above tungro
has become increasingly important since the mid-1960s, when planting of high-
yielding cultivars was started in the Asian tropics and double-cropping of rice
became common in irrigated areas. In most irrigated areas in the Asian tropics,
rice plantings are staggered and crop seasons are indefinite. This condition is
favorable for tungro and the vector N. virescens. Use of high-yielding cultivars
with similar genetic backgrounds over wide geographic areas also favored the
development of populations of vectors adapted to the cultivars (28, 58).
An outbreak of rice waika virus (RTSV) occurred in 1971–1974 in Kyushu,
Japan (43, 131). An abnormality similar to waika had been observed in rice
in Kyushu since 1964. The high incidence of rice waika virus in 1971–1974
was attributed to higher winter temperatures in 1972 and 1973 and to use of a
rice cultivar that is highly susceptible to the virus and that was planted widely
in Kyushu during this period. More waika-infected rice stubble overwinters
in Kyushu if winter temperatures are higher (72). The incidence of waika
declined to a low level and eventually disappeared in most places after 1975.
The decline was attributed to low winter temperatures in 1974; replacement
of the susceptible cultivar with nonsusceptible cultivars; and lower density of
N. cincticeps due to insecticide application in seedling boxes and to intensified
plowing of fallow rice fields (43, 130).
Rice Yellow Mottle Virus
Rice yellow mottle virus (RYMV) is a member of the sobemovirus group (7,
8). The virus particles are polyhedral, about 30 nm in diameter, and contain
one molecule of ssRNA and one protein. Infected rice plants show mottling
or yellow-orange discoloration of leaves, stunting, and sterility. In infected
266 HIBINO
rice cells, virus particles are scattered or aggregated in crystalline arrays in the
cytoplasm. Infected cells contain long flexuous tubules, 10–15 nm in diameter,
and aggregates of fibrils in the cytoplasm. Virus concentration is high in infected
rice tissues.
RYMV is transmitted in a semipersistent manner by a number of chrysomelid
beetles, including Sesselia pussilla, Chaetocnema pulla, and Trichispa sericea
(7, 8). It is mechanically transmissible and can also be transmitted by the long-
horned grasshopper Conocephalus merumontanus. S. pussilla is an efficient
vector, whereas C. pulla and T. sericea are less efficient but occur abundantly
in rice fields. RYMV is not circulative in the vector beetles, which retain the
virus for 1–8 days, with an average of 2–3 days.

RYMV naturally infects the wild species Oryza longistaminata in Niger and
Mali (77), and perhaps elsewhere (39). In Nigeria, however, infection of the
wild rice has not been confirmed (123). The role of the wild rice as the source
for spreading RYMV is not known. Four grasses, Dinebra retroflexa, Eleusine
indica, Eragrostis tenuifolia, and an Oryza species, sustained an infection with
RYMV when planted in rows alternatively with artificially infected rice plants
(114).
RYMV occurs in irrigated paddies, inland swamps, deep-flooded rice, and in
upland rice (121). The incidence is generally high in irrigated areas where more
than one crop of rice is planted. In such areas, infected rice stubble is the major
source of RYMV. The virus spreads from the source to other plants mainly by
mechanical means with the aid of harvesting stickers or through contacts via
injury, and also by vector beetles. As virus concentration is high in infected
tissues, incorporation of infected plants or their sap into soil or into flood water
facilitates infection of newly transplanted seedlings. Yellow mottle–infected
plants appear two to three weeks after transplanting as patches along the edges
and in the field. The patches enlarge and may fuse with each other and eventually
cover a large area. The incidence of RYMV is generally high during the rainy
season. RYMV was first observed in Kenya in 1966, and subsequently, during
1976 to 1983, was found in many rice-growing countries of Africa, including
Burkina Faso, Ghana, Ivory Coast, Kenya, Liberia, Mali, Niger, Nigeria, Sierra
Leone, and Tanzania. In 1989, it was found in Madagascar (122).
CONCLUSION
Many of the 15 rice viruses, especially planthopper- or leafhopper-borne viruses,
have reached epidemic proportions in many countries and have caused serious
damage in rice. Major outbreaks of the hopper-borne viruses were generally
associated with high densities of their vectors. Although many virus diseases
have not been well analyzed, a number of outbreaks were attributed to major
changes in cultivation practices.
For example, before 1950 in Japan, wheat and barley were planted in paddy
fields during the winter season, and rice seedlings were raised in nursery beds
and transplanted in June or July after the winter cereals had been harvested. Un-
der this cropping system, rice virus diseases, except rice dwarf and rice stripe,
were not recognized as threats to rice production. RDV and RSV were endemic
in localized areas of southern and central Japan and sometimes even reached
epidemic levels. Since 1950, major changes in rice cropping systems have had
an enormous impact on diseases and insect pests, especially on hopper-borne
virus diseases in rice (81). The changes included increased areas planted for
early season rice, which was transplanted in late April to May; reduction in ar-
eas planted for the winter cereals from 1.8 million ha in 1950 to 0.9 in 1965 and
to 0.2 in 1975; and the introduction of machine transplanters using seedlings
prepared in nursery boxes under a controlled environment. The early planting
increased the probability of stable yields and decreased potential damage from
typhoons. The reduction in growth of winter cereals was mainly due to in-
creases in the cost of production, which increased the importation of low-price
cereals. The introduction of early rice and early planting of middle-season rice
created a sequence of crops starting from late April, and provided a continu-
ous source of young seedlings for the viruses and for the first and the second
generations of their vectors N. cincticeps and L. striatellus. The application of
fertilizer increased substantially after 1950, producing conditions favorable for
both the viruses and their vectors. As a result, virus incidence, vector popula-
tion, and the percentage of virus infective hoppers in overwintering populations
all increased dramatically (81). The conditions were also favorable for another
L. striatellus-borne virus, RBSDV, and for a N. cincticeps-borne rice yellow
dwarf phytoplasma (81). The epidemics of RSV and RDV, which are trans-
mitted through eggs, lasted over ten years, but that of RBSDV and rice yellow
dwarf phytoplasmas eased in three to four years. Epidemics where the virus is
transmitted via vector eggs persist long after the environment has become less
favorable for the virus and for its vector (86).
The introduction of machine transplanters also affected disease incidence
in Japan. RNMV disappeared after their introduction. The use of nursery
boxes provided an effective control option for hopper-borne viruses, through
the appplication of insecticides in the nursery. On the other hand, use of nursery
boxes facilitated the spread of certain seed-borne fungal and bacterial diseases
that had not been serious problems in rice production hitherto (118).
In China, major outbreaks of rice viruses were recorded after 1963, when
double-cropping of rice became common in southern China and total production
started to greatly increase (FAO Statistics). The outbreaks were attributed to
increased double-cropping and early planting of the first-crop rice, and to the
application of fertilizers (143, 146). The epidemics of RBSDV in 1963–1967
were attributable to increased wheat cultivation (143).
268 HIBINO
In the Asian tropics, the first high-yielding semi-dwarf cultivar was bred at
IRRI and released in the mid-1960s (52). High-yielding cultivars have subse-
quently been planted widely in the Asian tropics and have been used as parents
in the rice breeding programs in many countries (50). Cultivar improvement has
had an enormous impact on Asian agriculture and has resulted in a remarkable
increase in rice yield and total rice production in Asia, especially in tropical
regions (38, 52). This change is known as “The Green Revolution.” Before
high-yielding cultivars were introduced, rice cultivars planted were tall, low
tillering, required short days for flowering, and needed a long period of growth
(five or six months) to mature. The taller traditional rice lodged if nitrogen
fertilizer was applied, and it was planted in the monsoon season. The high-
yielding cultivars are short and photo-insensitive, have higher tillering ability,
and a shorter growing season of four months. The use of improved cultivars
allows more than two crops a year to be planted, if sufficient irrigation is avail-
able. Since the 1960s, double-cropping of rice has become popular in irrigated
areas and the application of fertilizer has increased greatly. As a result, rice
planting is staggered in irrigated areas, and rice exists all year round. Also,
there is strong tendency for planting wide areas with rice cultivars having simi-
lar genetic background. Such conditions are favorable to rice viruses and their
vectors. In the Asian tropics, many virus diseases and their vectors, not recog-
nized previously as problems in rice production, have become major threats to
the stable production of rice.
In Latin America, the high incidence of RHBV was attributed to a large in-
crease in the density of vectors after improved rice cultivars were introduced,
which allowed double-cropping of rice (45). Although the pathogenic virus is
not hopper-borne, the incidence of RYMV in Africa is generally high in irri-
gated areas where rice is planted year round (136). It is likely that RHBV and
RYMV, which are indigenous in Latin America and Western Africa, respec-
tively, have become serious pests after the introduction of the new rice cultivars
and intensification of rice-cropping systems (135).
Rice has a long history of cultivation in Asia, spanning from 2000 to 4000
years. Many rice viruses have probably long been in the equilibrium stage
established between host and pathogen in each area (136). This balance was
disrupted by the recent intensification of cropping systems, including the in-
troduction of double-cropping and the application of fertilizer, which greatly
increased rice yield and total rice production in many countries. It would not
be practical to change the rice-cropping system extensively again to deal with
problems caused by viruses and other pests. Indeed, the level of production
achieved over the past three decades is still insufficient to support the burgeon-
ing population, and it has to be increased even further. The development of
ecologically sound management practices to deal with rice virus diseases in the
double-cropping system is critical. Fortunately, in some countries in higher
latitudes in Asia, the incidence of virus diseases in rice has generally been low
for over ten years, indicating the possible establishment of a new equilibrium
between rice and pathogen. In the Asian tropics, management practices in-
corporating a definite fallow period after each crop season in each area have
been successful in managing rice tungro disease (125). In such areas, the tun-
gro viruses are apparently endemic and do not cause economic losses. More
research is needed on the epidemiology of rice viruses in relation to cropping

systems so that effective management strategies can be implemented.
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Annual Review of Phytopathology
Volume 34, 1996
CONTENTS
PLANT PATHOLOGY: A Discipline at a Crossroads, Albert R.
Weinhold 1
HELEN HART, REMARKABLE PLANT PATHOLOGIST
(1900–1971), Roy D. Wilcoxson 13
DR. GOTTHOLD STEINER (1886–1961): VERSATILE
NEMATOLOGIST, Robert P. Esser 25
THE RED QUEEN HYPOTHESIS AND PLANT/PATHOGEN
INTERACTIONS, Keith Clay, Paula X. Kover 29
THE ROLE OF PLANT CLINICS IN PLANT DISEASE DIAGNOSIS
AND EDUCATION IN DEVELOPING COUNTRIES, Reuben Ausher,
Israel S. Ben-Ze'ev, Robert Black 51
DWARF BUNT: Politics, Identification, and Biology, D. E. Mathre 67

FUNGAL TRANSMISSION OF PLANT VIRUSES, R. N. Campbell 87
EPICHLOË SPECIES: Fungal Symbionts of Grasses, Christopher L.

Schardl 109
FASTIDIOUS XYLEM-LIMITED BACTERIAL PLANT
PATHOGENS, Alexander H. Purcell, Donald L. Hopkins 131
BACTERIAL AVIRULENCE GENES, Jan E. Leach, Frank F. White 153
CHEMORECEPTION IN PLANT PARASITIC NEMATODES, Roland
N. Perry 181
NEMATODE MANAGEMENT IN SUSTAINABLE AND
SUBSISTENCE AGRICULTURE, J. Bridge 201
HELPER-DEPENDENT VECTOR TRANSMISSION OF PLANT
VIRUSES, Thomas P. Pirone, Stéphane Blanc 227
BIOLOGY AND EPIDEMIOLOGY OF RICE VIRUSES, Hiroyuki
Hibino 249
MOLECULAR BIOLOGY OF RICE TUNGRO VIRUSES, Roger Hull 275
PLANT VIRUS GENE VECTORS FOR TRANSIENT EXPRESSION
OF FOREIGN PROTEINS IN PLANTS, Herman B. Scholthof, Karen-
Beth G. Scholthof, Andrew O. Jackson 299
ROOT SYSTEM REGULATION OF WHOLE PLANT GROWTH, R.
M. Aiken, A. J. M. Smucker 325
OZONE AND PLANT HEALTH, Heinrich Sandermann Jr 347
MORPHOGENESIS AND MECHANISMS OF PENETRATION BY
PLANT PATHOGENIC FUNGI, K. Mendgen, M. Hahn, H. Deising 367
MICROBIAL ELICITORS AND THEIR RECEPTORS IN PLANTS,
Michael G. Hahn 387
PATHOGEN QUIESCENCE IN POSTHARVEST DISEASES, Dov
Prusky 413
GENETICS OF RESISTANCE TO WHEAT LEAF RUST, J. A. Kolmer 435

RECOMBINATION AND THE MULTILOCUS STRUCTURE OF
FUNGAL POPULATIONS, Michael G. Milgroom 457
QTL MAPPING AND QUANTITATIVE DISEASE RESISTANCE IN
PLANTS, N. D. Young 479
BREEDING DISEASE-RESISTANT WHEATS FOR TROPICAL
HIGHLANDS AND LOWLANDS, H.J. Dubin, S. Rajaram 503
CHANGING OPTIONS FOR THE CONTROL OF DECIDUOUS
FRUIT TREE DISEASES, Turner B. Sutton 527
RESISTANCE TO PHENYLAMIDE FUNGICIDES: A Case Study with
Phytophthora infestans Involving Mating Type and Race Structure, U.
Gisi, Y. Cohen 549
STATUS OF CACAO WITCHES' BROOM: Biology, Epidemiology, and
Management, LH Purdy, RA Schmidt 573

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July 10, 1996 17:9 Annual Reviews HIBINO.

Annu. Rev. Phytopathol. 1996. 34:249–74

BIOLOGY AND EPIDEMIOLOGY

Chugoku National Agricultural Experiment Station, Nishifukatsu 6-12-1, Fukuyama,

KEY WORDS: rice viruses, biology, transmission, infection cycle, epidemiology

rice yield was low.

BIOLOGY AND EPIDEMIOLOGY

EPIDEMIOLOGY OF RICE VIRUSES 251

and maize in 1965–1967. In China, an outbreak occurred in 1963 and in 1965–

Rice Dwarf Virus

the family Reoviridae. The virus particles are polyhedral, about 70 nm in

EPIDEMIOLOGY OF RICE VIRUSES 253

rice fields. The percentage of infective N. cincticeps in the populations is high

Rice Gall Dwarf Virus

pertrophy of the phloem tissues. In infected plants, RGDV is localized in the

or scattered in or around viroplasmic inclusions, or arranged in tubules in the

Rice Giallume Virus

EPIDEMIOLOGY OF RICE VIRUSES 255

membraned vesicles with fibrils, degenerated mitochondria, and deposits of

rice. RGV overwinters in L. orizoides. In rice fields, L. orizoides develops new

RGSV naturally infects only rice. The vector N. lugens is monophagous

lugens, and in addition from rice ragged stunt virus.

EPIDEMIOLOGY OF RICE VIRUSES 257

tenuivirus group. The virus-specific protein of RHBV is serologically related

of the virus in S. orizicola, planthoppers that acquire RHBV through feeding

reduced number of tillers; a spreading growth habit; elongated or spindle-

EPIDEMIOLOGY OF RICE VIRUSES 259

RRSV is transmitted in a persistent manner by the brown planthopper, Nila-

Rice Stripe Necrosis Virus

nis. However, it is also mechanically transmissible.

Rice Stripe Virus

EPIDEMIOLOGY OF RICE VIRUSES 261

RTYV is transmitted in a persistent manner by Nephotettix cincticeps, N.

is not transmitted via eggs. Vector efficiency is high in N. cincticeps and

EPIDEMIOLOGY OF RICE VIRUSES 263

Rice Tungro Bacilliform and Rice Tungro Spherical Viruses

(61). Discolored leaves may show irregularly shaped dark-brown blotches.

EPIDEMIOLOGY OF RICE VIRUSES 265

scheduled to have nearly synchronous growth and to maintain a definite fallow

virus for 1–8 days, with an average of 2–3 days.

EPIDEMIOLOGY OF RICE VIRUSES 267

EPIDEMIOLOGY OF RICE VIRUSES 269

research is needed on the epidemiology of rice viruses in relation to cropping

1. Amici A, Faoro F, Osler R, Tornaghi R. 4 pp.

EPIDEMIOLOGY OF RICE VIRUSES 271

Transmission of rice necrosis mo- plants and vector leafhoppers. In Patho-

Japanese) the rice stripe virus. Virology 32:144–52

grassy stunt virus in various colonies of planthopper-rice virus epidemiology

EPIDEMIOLOGY OF RICE VIRUSES 273

102. Miyai S, Kiritani S, Nakasuji F. 1986. 114

planthopper Laodelphax striatellus 139. Toriyama S. 1995. Viruses and molecu-

DWARF BUNT: Politics, Identification, and Biology, D. E. Mathre 67

EPICHLOË SPECIES: Fungal Symbionts of Grasses, Christopher L.

GENETICS OF RESISTANCE TO WHEAT LEAF RUST, J. A. Kolmer 435

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