September 1998
Family: Bunyaviridae
Genus: Tospovirus

Tospovirus genus

R. Kormelink
Department of Virology, Wageningen Agricultural University, Binnenhaven 11, 6709 PD, Wageningen, The Netherlands

D. Peters
Department of Virology, Wageningen Agricultural University, Binnenhaven 11, 6709 PD, Wageningen, The Netherlands

R. Goldbach
Department of Virology, Wageningen Agricultural University, Binnenhaven 11, 6709 PD, Wageningen, The Netherlands


Type Member
Main Characteristics
Geographical Distribution etc
Association with Vectors
Relations with Cells and Tissues
Particle Properties
Genome Properties
Defective-Interfering RNA
Relationships within the Taxon
Notes on Tentative Members
Affinities with Other Groups

Type Member

Tomato spotted wilt virus (TSWV).

Main Characteristics

Particles of tospoviruses are spherical and membrane-bound with a diameter of approximately 80-120 nm (Fig.1), and sediment at 530-583 S (s20,w; Best, 1968; Black, Brakke & Vatter, 1963). The viruses possess a tripartite ssRNA genome of which one segment is of negative polarity and the other two are ambisense. The virus particles are unstable, with a thermal inactivation point (10 min) of 40-46°C, a longevity in vitro at room temperature of 2-5 h and a dilution end-point between 2 x 10-2 and 1 x 10-4. During purification the viruses are greatly stabilized by the addition of reducing agents such as 0.01 M Na2SO3. For TSWV, yields are usually about 100-500 µg per 100 g leaf material of Nicotiana rustica. In infected cells, mature virus particles are found in the lumen of the endoplasmic reticulum. The viruses replicate in the cytoplasm where, with some isolates, fibrous inclusion bodies can be observed. Tospoviruses are transmitted in nature by various thrips species (Thysanoptera: Thripidae). They can also readily be transmitted by mechanical inoculation. Recent reviews on tospoviruses are by Goldbach & Peters (1994, 1996) and Mumford, Barker & Wood (1996).


To date, 11 definitive members of the tospovirus genus have been established, and several tentative members are proposed (Table 1; Adam et al., 1993; Cortes et al., 1998; De Ávila et al., 1990, 1993; Goldbach & Kuo, 1996; Heinze et al., 1995; Law & Moyer, 1990; Law, Speck & Moyer, 1991; Murphy et al., 1995; Reddy et al., 1992; Satyanarayana et al., 1996; Yeh & Chang, 1995; Yeh et al., 1992).

Geographical Distribution etc

TSWV, the type species of the genus Tospovirus, occurs worldwide, because of its wide plant host range and the worldwide distribution of its main vector, the thrips Frankliniella occidentalis. Other members of the Tospovirus genus appear more restricted in their distribution (Table 1). Generally, tospoviruses are widespread in tropical, subtropical and temperate climate zones. In the latter, however, they often prevail only in greenhouse cultivations.

Table 1 Geographical distribution, host range and vectors of tospoviruses

Virus Geographical distribution Host range Vector
Definitive species
Tomato spotted wilt virus (TSWV)17 worldwide10 Very broad (800 species) Frankliniella fusca 23
F. intonsa 30
F. occidentalis 9
F. schultzei 24, 30
Thrips palmi 8
T. setosus 8
T. tabaci 19
Impatiens necrotic spot virus (INSV)5, 15 USA15, Europe5, 16, 27 Mainly ornamentals, e.g.
begonia, dahlia,
exacum, gloxinia,
F. occidentalis 3, 29
Tomato chlorotic spot virus (TCSV)6 Brazil4 Tomato F. intonsa 30
F. schultzei 30
F. occidentalis 30
Groundnut ringspot virus (GRSV)6 Argentine7, Brazil4, South Africa Groundnut, tomato F. occidentalis 30
F. schultzei 30
Watermelon silver mottle virus (WSMV)13, 31 Japan14, Taiwan13, 31 Watermelon, other cucurbits T. palmi 32
Groundnut* bud necrosis virus (GBNV)21, 25 India21, South-East Asia Groundnut T. palmi 18, 28
F. schultzei ?18, 28#
Iris yellow spot virus(IYSV)2 The Netherlands Iris unknown
Melon spotted wilt virus(MSWV)34 Japan34 Melon T. palmi
Groundnut* yellow spot virus (GYSV)20 India, Thailand20 Groundnut unknown
Isolate Chry1 (no species name coined yet)22 Brazil22 Chrysanthemum, tomato unknown
Isolate BR-09Z22 (no species name coined yet) Brazil22 Zucchini unknown
Tentative species
Br-10 (Onion)22 Brazil22 Onion unknown
Groundnut* chlorotic fan- spot virus (GCFV)1 Taiwan1 Groundnut unknown
Tospovirus (Onion)11 USA (Idaho, Oregon)11 Onion unknown
Tospo-PD233 Taiwan33 Groundnut unknown
Tospovirus (Verbesina alternifolia)12 USA12 Verbesina alternifolia unknown
TSWV-W26 India26 Watermelon unknown

*: In literature GBNV is also named peanut bud necrosis (PBNV), GYSV also peanut yellow spot virus (PYSV) and GCFV also peanut chlorotic fan-spot virus (PCFV).#: F. schultzei later correctly identified as T. palmi (Palmer et al., 1990), no transmission of GBNV by F. schultzei (Vijayalakshmi, 1994).
References: 1 Chen & Chiu, 1996, 2 Cortes et al., 1998, 3 De Angelis, Sether & Rossignol, 1994, 4 De Ávila et al., 1990, 5 De Ávila et al., 1992, 6 De Ávila et al.,1993, 7 Dewey et al., 1993, 8 Fujisawa,Tanaka & Ishii, 1988, 9 Gardner, Tompkins & Whipple, 1935, 10 Goldbach & Peters, 1994, 11 Hall et al.,1993, 12 Hayati el al., 1990, 13 Heinze et al., 1995, 14 Kameya-Iwaki et al., 1984, 15 Law & Moyer, 1990, 16 Marchoux, Gebreselassie & Villevieille,1991, 17 Murphy et al., 1995, 18 Palmer et al., 1990, 19 Pittman, 1927, 20 Reddy et al., 1990, 21 Reddy et al., 1992, 22 Resende et al., 1996, 23 Sakimura, 1963, 24 Samuel, Bald & Pittman, 1930, 25 Satyanarayana et al., 1996, 26 Singh & Krishnareddy, 1996, 27 Vaira et al., 1993, 28 Vijayalakshmi, 1994, 29 Wijkamp & Peters, 1993, 30 Wijkamp et al., 1995, 31 Yeh & Chang, 1995, 32 Yeh et al., 1992, 33 Yeh et al., 1996, 34 Unpublished results from K. Kato., Shizuoka Agric. Exp. St., Shizuoka 438, Japan , quoted by Goldbach & Kuo, 1996.

More than 800 different plant species, from 82 botanical families, including both monocotyledonous and dicotyledonous plants, have been reported to be susceptible to TSWV (Peters, http://www.spg.wau.nl/viro). The virus causes great yield losses in a large number of economically important crops, e.g. groundnut, lettuce, papaya, pea, potato, sweet pepper, tobacco, tomato, and in ornamental crops, such as alstroemeria, begonia, chrysanthemum, cyclamen, dahlia, gerbera, gloxinia and impatiens. Disease symptoms range from chlorosis, mottling, stunting and wilting to severe necrosis of leaf and stem tissues. However, symptoms may vary within a host species according to the condition and age of the plant itself, as well as environmental conditions.

Association with Vectors

Under natural conditions, tospoviruses are spread by thrips. Seven thrips species (Thysanoptera: Thripidae) have been recorded as vectors of tospoviruses (Table 2; De Angelis, Sether & Rossignol, 1994; Fujisawa, Tanaka & Ishii, 1988; Gardner, Tompkins & Whipple, 1935; Kobatake, Osaki & Inouye, 1984; Palmer et al., 1990; Pittman, 1927; Sakimura, 1963; Samuel, Bald & Pittman, 1930; Umeya, Kudo & Miyazaki, 1988; Vijayalakshmi, 1994; Wijkamp et al., 1995; Wijkamp & Peters, 1993; Yeh et al., 1992). TSWV is transmitted by most, if not all of these species. Since 1980, a rapid spread of the western flower thrips, F. occidentalis, has contributed to a worldwide resurgence of TSWV. Factors that have contributed to this are the concealed way of life and short life cycle of this thrips species, its ability to colonize many weed and cultivated plant species, its increased tolerance to insecticides and the global trading of thrips-infested plant material.

Table 2 Geographical distribution and host range of reported tospovirus vectors

Thrips species Geographical distribution Host
Frankliniella fusca Hinds11
(tobacco thrips)
Widespread throughout North America and Mexico9,11 Polyphagous; common on cotton, grasslands, groundnut, tobacco9
F. intonsa Trybom14,17
(flower thrips)
Palaearctic, widespread throughout Asia, CIS and Europe. Also reported from India and USA9,14 Polyphagous (flowers); alfalfa, clover, many ornamentals and vegetables14
F. occidentalis Pergande7
(western flower thrips, alfalfa thrips, California thrips)
Widespread throughout Europe, Hawaii, North and Central America, and New Zealand. Also reported from Argentina, Asia, Australia, CIS and South Africa4,6 Polyphagous (flowers); cotton, many fruits, ornamentals, seed crops and vegetables1,4,9
F. schultzei Trybom12
(cotton bud thrips, common blossom thrips)
Tropics, widespread throughout Africa, Asia, Australia, Caribbean, Pacific and South America. Also reports from Florida and temperate climate zones (introduced); Great Britain, Italy, The Netherlands15 Polyphagous (flowers); chilli, cotton, Compositae, groundnut, mung bean, onion, pigeon pea, sorghum and tomato9
Thrips palmi Karny18
(melon thrips)
Tropics, widespread throughout Asia, Carribean, Central America, Northern Australia and Pacific. Also reported from Florida, Guyana, Nigeria, Sudan and Venezuela. Temperate climate zones; Finland, The Netherlands3,5 Polyphagous; cotton, cucurbits, Leguminosae and Solanaceae3,9,13,16
T. setosus Moulton8 Japan, Korea9,14 Polyphagous; cowpea, cucumber, dahlia, narcissus, soybean, strawberry, sweet pepper, tea, tomato, watermelon14
T. tabaci Lindeman10
(onion thrips)
Worldwide, widespread on all continents2 Polyphagous; cabbage, cotton, onion, ornamentals, tobacco, vegetables 9,13

References: 1 Brødsgaard, 1989, 2 CAB, 1969, 3 CAB, 1992, 4 CAB, 1993, 5 Cermeli & Montagne, 1993, 6 Dal Bó et al., 1995, 7 Gardner, Tompkins & Whipple, 1935, 8 Kobatake, Osaki & Inouye, 1984, 9 Palmer, Mound & Du Heaume, 1992, 10 Pittman, 1927, 11 Sakimura, 1963, 12 Samuel, Bald & Pittman, 1930, 13 Talekar, 1991, 14 Umeya, Kudo & Miyazaki, 1988, 15 Vierbergen & Mantel, 1991, 16 Walker, 1994, 17 Wijkamp et al., 1995, 18 Yeh et al., 1992.

Transmission occurs in a propagative manner (Wijkamp et al., 1993; Ullman et al., 1993). The virus is acquired only by the first (L1) and second (L2) larval stages and can readily be transmitted in the L2 and adult stages (Van de Wetering, Goldbach & Peters, 1996; Wijkamp & Peters, 1993). For F. occidentalis, the acquisition access period (AAP50) and inoculation access period (IAP50) needed for 50% of the thrips to acquire and inoculate TSWV are 67 min and 59 min, respectively. The median latent period (LP50) decreases with increasing temperature, and ranges between 80 and 170 h (Wijkamp & Peters, 1993; Wijkamp, 1995). Once the virus is acquired, it is passed trans-stadially and thrips remain infectious for life.

Relations with Cells and Tissues

Data in this section are based on the observations made on TSWV, and thus far seem to apply for all tospoviruses, except where indicated. TSWV is found in almost all tissues and organs following systemic infection of plants (Ie, 1973; Francki & Grivell, 1970; Kitajima, 1965; Kitajima et al., 1992). Mature virus particles accumulate mainly in clusters in the cisternae of the rough endoplasmic reticulum (RER) and consist of spherical lipid-bound particles, 80-120 nm in diameter, covered with spike projections (Best & Palk, 1964; Best & Katekar, 1964; Francki & Grivell, 1970; Francki & Hatta, 1981; Francki, Milne & Hatta, 1984; Ie, 1964; Kitajima, 1965; Martin, 1964; Van Kammen, Henstra & Ie, 1966).

In addition to mature virus particles, specific cytopathic structures are associated with TSWV infection. One type is characterized by dark diffuse amorphous masses, sometimes called viroplasms, with locally electron-dense striated spots, dispersed freely in the cytoplasm (Francki and Grivell, 1970; Francki and Hatta, 1981; Francki, Milne & Hatta, 1984; Ie, 1971; Kitajima, 1965; Kitajima et al., 1992; Milne, 1970). The electron-dense spots have a diameter slightly smaller than that of mature virus particles (Ie, 1971), and are proteinaceous in nature; they are suggested to consist of ribonucleoprotein and to be a normal developmental stage in the formation of TSWV particles (Milne, 1970; Ie, 1971). This idea receives support from studies of morphologically defective TSWV isolates (Ie, 1982; Resende et al., 1991; Verkleij & Peters, 1983), in which purified infectious fractions of TSWV were found to resemble the amorphous masses in infected plant cells. It was therefore suggested that these masses consist of aggregates of nucleocapsids that are not enveloped, either because they are at an intermediate stage of development or because they represent morphologically defective TSWV that for some reason cannot produce enveloped particles (Ie, 1982; Resende et al., 1991; Verkleij & Peters, 1983).

The second type of cytopathic structure associated with tospovirus infections is fibrous (Francki and Grivell, 1970; Francki, Milne & Hatta, 1984; Kitajima et al., 1992; Kormelink et al., 1991) and consists of either elongated flexible filaments (TSWV) or more rigid rods (INSV) organized in a paracrystalline array. These structures have been shown to contain one of the non-structural proteins of TSWV, the NSS protein (Kitajima et al., 1992; Kormelink et al., 1991), but their precise nature and function remain unknown.

Sometimes, though only at an early stage of infection, doubly enveloped particles are found in the cytoplasm (Francki, Milne & Hatta, 1984; Kitajima et al., 1992; Milne, 1970). They are reported to arise as a result of budding of nucleocapsids from parallel membranes to form enveloped particles. It is hypothesized that subsequent joining of several doubly enveloped particles may lead to the formation of a cluster of singly enveloped particles in the cisternae of RER (Kitajima et al., 1992; Milne, 1970). Virus particles have not been observed in the Golgi complex or vacuoles, but information on the maturation or transport of the virus is still limited, possibly because the intermediate stages of particle budding are passed through rapidly.

During early stages of the infection, moreover, tubular structures have been observed extending from plasmodesmata into newly infected cells. These structures have been shown to be composed of another non-structural protein, NSM (Kormelink et al., 1994; Storms et al., 1995). Microinjection of fluorescent dyes into parenchyma cells of transgenic plants expressing this protein has shown that the size exclusion limit of plasmodesmata was modified (Storms et al., 1998). Hence, the NSM protein has been implicated in the cell-to-cell movement of non-enveloped infectious ribonucleocapsid structures of TSWV.

In viruliferous individuals of the thrips F. occidentalis, large amounts of the N and NSS proteins are found in the salivary glands. Additionally, both proteins are present in muscle cells associated with the midgut epithelium. Mature virus particles are observed in vesicles in the salivary glands, and in massive numbers in the salivary gland ducts, suggesting that the salivary glands are the major site of replication (Ullman et al., 1992, 1993; Wijkamp et al., 1993).

Particle Properties

TSWV, and all other members of the genus Tospovirus, have particles that are spherical and membrane bound (80-120 nm; Fig.1). The particles are covered with surface projections that consist of two glycoproteins, G1 (78 kDa) and G2 (58 kDa) (Mohamed, Randles & Francki, 1973; Tas, Boerjan & Peters, 1977). An additional smaller version of the G2 protein of about 52 kDa is often observed in purified TSWV preparations. The core consists of pseudo-circular ribonucleocapsids (Fig.2), each consisting of a viral RNA segment tightly wrapped in molecules of the nucleoprotein (N, 29 kDa) and minor amounts of a large protein (L, 331.5 kDa), the putative viral RNA polymerase (Mohamed, 1981; Tas, Boerjan & Peters, 1977; Van den Hurk, Tas & Peters, 1977; Van Poelwijk et al., 1993; Verkleij & Peters, 1983). The structural proteins of different tospoviruses differ slightly in size. For the N protein, reported sizes range between 28.7 and 30.7 kDa. Purified particles, as well as ribonucleocapsids, but not the RNA, are infective when inoculated onto plants. Only enveloped particles are transmitted by thrips (Resende et al., 1991; Wijkamp, 1995). Particles contain about 65% protein, 20% lipid, 7% carbohydrate and 5% RNA (Best, 1968).

Genome Properties

The complete nucleotide sequence of the tripartite genome of TSWV has been determined (De Haan et al., 1989, 1990, 1991; Kormelink et al., 1992a). A schematic representation of the genome organization of TSWV, is shown in Fig.3. This organization applies to all members of the tospovirus genus studied so far. The large (L) RNA segment contains 8897 nucleotides (nt), and is of negative polarity. The viral complementary (vc) strand contains one large ORF, encoding a protein of 331.5 kDa which, based on sequence homology with the Bunyamwera virus L protein and influenzavirus PB1 protein, is thought to represent the viral RNA-dependent RNA polymerase (De Haan et al., 1990). The medium-sized (M) RNA segment contains 4821 nt, and has an ambisense gene arrangement (Kormelink et al., 1992a). This RNA segment encodes in the viral (v) sense a non-structural protein (NSM) of 33.6 kDa, which is implicated in cell-to-cell movement (Kormelink et al., 1994; Storms et al., 1995, 1998), and in the vc sense a 127.4 kDa protein which is the precursor to the glycoproteins (G1 and G2). The small (S) RNA segment contains 2916 nt and, like the M RNA, has an ambisense gene arrangement. This genome segment encodes a non-structural (NSS) protein of 52.4 kDa in the v sense and the nucleoprotein (N) of 28.8 kDa in the vc sense (De Haan et al., 1990; Kormelink et al., 1991). The function of the NSS protein is unknown.

About 65-70 nt of the L, M and S RNA molecules are complementary at the 5' and 3' ends, and this results in the formation of stable ‘panhandle’ structures, causing the RNA segments to appear as pseudo-circular structures (Fig.2). The 5'- and 3'-terminal sequences of all three RNA segments are identical for the first eight nucleotides, a typical feature of negative-stranded, segmented RNA viruses (Orthomyxoviridae, Bunyaviridae, Arenaviridae, tenuiviruses); this is thought to have an important function in genome replication and transcription (De Haan et al., 1989). The non-coding intergenic regions of both the M and S RNA segments contain an internal inverted sequence of A- and U-rich stretches that can be folded into a hairpin structure. A conserved sequence (CAAACUUUGG) has been found at the top of the hairpin of the TSWV and INSV M and S RNA segments, suggesting a possible function in termination of transcription.


Little is known about the replication and transcriptional strategy of the tospoviral genome. Time-course experiments with (wild-type) TSWV-infected Nicotiana rustica plants (Kormelink et al., 1992b) have shown the synthesis of full-length L, M and S RNA molecules of v polarity (high amounts) and vc polarity (low amounts). No subgenomic RNA molecules derived from L RNA have been detected, suggesting that the mRNA for the L ORF is of almost full length. The M and S RNA segments each give rise to two subgenomic RNA molecules, transcribed from opposite strands. These RNA molecules are probably mRNAs, reflecting the ambisense gene arrangement of both segments (Kormelink et al., 1992a, 1992b; De Haan et al., 1990). Moreover, analysis of the RNA contents of the virus particles and nucleocapsid preparations has shown that these subgenomic mRNA molecules are not encapsidated into ribonucleocapsids and, as a result, are not present in virus particles. Viral (v) and vc strands of all three genomic RNA segments are found in virus preparations; the v strands are in excess over vc strands, possibly reflecting the difference in amounts synthesized in infected plants (Kormelink et al., 1992b). Primer extension and nucleotide sequence analyses of the subgenomic N, NSS and NSM mRNAs revealed the presence of heterogeneous non-viral sequences, 12-20 nt in length, at the 5'ends of the mRNA molecules (Kormelink et al., 1992c; Van Poelwijk, Kolkman & Goldbach, 1996), indicating that in TSWV ‘cap- snatching’ (Braam, Ulmanen & Krug, 1983; Plotch et al., 1981; Ulmanen, Broni & Krug, 1981) is probably the mechanism by which transcription of the viral genome is initiated. It has not been shown whether the endonuclease activity involved in cap- snatching is encompassed in the viral polymerase (L protein).

Defective-Interfering RNA

RNA molecules of subgenome length, derived from the L RNA, have been found repeatedly as a result of serial mechanical passages of TSWV at high inoculum concentration and low temperature regimes (Inoue-Nagata et al., 1997; Resende et al., 1991). These defective RNA molecules have been shown to interfere with the replication of the wild-type genome (Resende et al., 1991), and hence cause attenuation of symptom expression. All DI RNA molecules studied have been shown to retain the genomic 5' and 3' ends, suggesting that these sequences are essential for replication, encapsidation and subsequent packaging into virus particles (Resende et al., 1992). The mode by which the internal deletions are generated is unknown.

Relationships within the Taxon

Tospovirus species are distinguished on the basis of N protein serology, N protein sequences and vector specificity (Goldbach & Kuo, 1996). Currently, 11 established species are recognized and clustered into four distinct serogroups, with the aid of polyclonal and monoclonal antisera directed to the viral nucleoproteins (Cortes et al., 1998; De Ávila et al., 1990; Goldbach & Kuo, 1996; Law & Moyer, 1990). Serogroup I is represented by TSWV. Tomato chlorotic spot virus (TCSV) and groundnut ringspot virus (GRSV) are in serogroup II. For serogroups III and IV, the proposed representatives are, respectively, impatiens necrotic spot virus (INSV) and groundnut bud necrosis virus (GBNV). Two newly analysed tospoviruses, denoted iris yellow spot virus (IYSV) and groundnut yellow spot virus (GYSV), are proposed as representative of serogroup V (Cortes et al., 1998) and VI (Satyanarayana et al., 1998), respectively. Other isolates may in the near future be recognized as new distinct species of the tospovirus genus (Table 1). For eight species, complete N protein gene sequences are available (Table 3: Cortes et al., 1998; De Ávila et al., 1993; De Haan et al., 1990; Heinze et al., 1995; Law & Moyer, 1990; Satyanarayana et al., 1996, 1998; Yeh et al., 1992) and subsequent multiple alignment confirmed the interrelationships among them (Fig.4). On a higher taxonomic level, there is no serological relationship between tospoviruses and members from other genera of the family Bunyaviridae. However, a low but significant level of amino acid sequence homology was found for the precursor to the glycoproteins and for the RNA polymerase between TSWV and members of the Bunyavirus genus (De Haan et al., 1991; Kormelink et al., 1992a).

Table 3 Amino acid sequence identities (%) of tospoviral N proteins

  Serogroup I Serogroup II Serogroup III Serogroup IV Serogroup V Serogroup VI
TSWV 100 78 77 55 33 33 34 26
GRSV   100 81 54 34 33 33 22
TCSV     100 55 33 26 34 23
INSV       100 30 30 30 23
GBNV         100 85 44 24
WSMV           100 44 23
IYSV             100 21
GYSV               100

1  De Haan et al., 1990 (GenBank accession number D00645); 2  De Ávila et al., 1993 (access. nr. S54325 and S54327); 3  De Haan et al., 1992 (access. nr. X66972); 4  Law & Moyer, 1990 (access. nr. D00914); 5  Satyanarayana et al., 1996 (access. nr. U27809); 6  Heinze et al., 1995 (access. nr. Z46419); 7  Yeh & Chang, 1995 (access. nr. X78556/U78734); 8  Cortes et al., 1998 (access. nr. AF001387); 9  Satyanarayana et al., 1998 (access. nr. AF013994).


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Figure 1

Electron micrograph of purified TSWV particles. Scale bar represents 100 nm.

Figure 2

Electron micrograph of purified TSWV ribonucleocapsids. Scale bar represents and 10 nm.

Figure 3

The genome structure and expression strategy of the tripartite genome of TSWV. Boxes represent ORFs, and circles indicate non-viral sequences used to initiate transcription of the viral mRNAs.

Figure 4

Phylogenetic tree of tospoviruses based on the amino acid homology of their nucleoprotein. Sequences were derived from Cortes et al., 1998 (IYSV); De Ávila et al., 1993 (GRSV, TCSV); De Haan et al., 1990 (TSWV); Heinze et al., 1995 (WSMV); Law, Speck & Moyer, 1991 (INSV); Satyanarayana et al., 1996 (GBNV); Satyanarayana et al., 1998 (GYSV).