Details of DPV and References
DPV NO: 295 July 1984
Species: | Acronym:
R. Hull John Innes Institute, Colney Lane, Norwich NR4 7UH, UK
- Type Member
- Main Characteristics
- Geographical Distribution
- Transmission by Vectors
- Ecology and Control
- Relations with Cells and Tissues
- Properties of Particles
- Genome Properties
- Defective-Interfering RNA
- Notes on Tentative Members
- Affinities with Other Groups
cauliflower mosaic virus
Caulimoviruses have isometric particles 45-50 nm in diameter which sediment at 215-245 S. The particles contain a single molecule of dsDNA which has a M. Wt of c. 5 x 106 (7.8-8.0 kbp) and comprises about 17% of the particle weight. There is a single species of coat protein which is proteolysed in vivo and in vitro to give M. Wt (x 10-3) of 35-42. Thermal inactivation points are 80-90°C, dilution end-points about 10-3 and longevity in sap is up to 7 days (20°C). The particles occur in characteristic cytoplasmic inclusion bodies, the matrix of which is predominantly a virus-coded protein of about 62,000 M. Wt. Caulimoviruses are transmitted by inoculation with sap. Their natural mode of transmission, where known, is by aphids in a non-persistent or semi-persistent manner; a virus-coded protein is needed to facilitate aphid-transmission. The host ranges are relatively narrow.
|Diameter (nm)||Particle sedim. coefft
|CsCl banding density (g/cm3)||Coat protein M. Wt x 10-3||DNA||DPV no. or reference|
|Size(kbp)||No. of disconti-
|Cauliflower mosaic (CaMV)|
|Cr (So)||Aphids||50||208||1.35||42(65, 37,35)||8.0||3 or 2||243|
|Carnation etched ring (CERV)|
|Dahlia mosaic (DaMV)|
|Co (Am) (So) (Ch)||Aphids||48-50||254||-||-||8.0||3 or 4||51,c,d|
|Figwort mosaic (FMV)|
|Horseradish latent (HRLV )|
|Mirabilis mosaic (MMV)|
|Soybean chlorotic mottle (SoyCMV)|
|Strawberry vein banding (SVBV)|
|Thistle mottle (ThMV)|
|Blueberry red ringspot (BRRV)|
|Cassava vein mosaic (CVMV)|
|Cestrum virus (CV)|
|Petunia vein clearing (PVCV)|
|Plantago virus 4 (P1V4)|
* Families in parentheses indicate laboratory infections. Abbreviations for families:- Am = Amaranthaceae; Ca = Caryophyllaceae; Ch = Chenopodiaceae; Co = Compositae; Cr = Cruciferae; Er = Ericaceae; Eu = Euphorbiaceae; Le = Leguminosae; Ny = Nyctaginaceae; Pl = Plantaginaceae; Ro = Rosaceae; Sc = Scrophulariaceae; So = Solanaceae
** ND = not determined.
References, a. Hull & Donson (1982); b. R. Hull (unpublished data); c. Richins & Shepherd (1983); d. J. Donson (unpublished data); e. Shepherd & Lawson (1981); f. Handley, Duffus & Shepherd (1982); g. Brunt & Kitajima (1973); h. Donson & Hull (1983); i. Iwaki et al., (1984); j. Kim et al., (1981); k. Kitajima & Costa (1966); l. Lin & Kitajima (1980); m. Ragozzino (1974); n. Lesemann & Casper (1973); o. Hammond (1981); p. Hammond (1982).
It is uncertain whether HRLV is distinct from CaMV.
CaMV, CERV and DaMV are widely distributed, probably occurring throughout the geographical ranges of their respective hosts. FMV, MMV and BRRV are reported only from restricted regions in North America; ThMV, CV, PVCV and PlV4 from restricted regions in Europe; CVMV from South America; SoyCMV from Japan; and SVBV from North America and Europe. Host ranges are limited to the families given in Table 1; those of some members are limited to one or two genera.
Transmission by Vectors
CaMV, CERV, DaMV, FMV, MMV and SVBV are transmitted by aphids in a non-persistent or semi-persistent manner; the modes of transmission of other caulimoviruses are unknown. Most of the above viruses are transmitted by several aphid species (e.g. CaMV by 27 spp.; Kennedy, Day & Eastop, 1962). The viruses are acquired during short acquisition feeds (1 min) and can be inoculated immediately. Aphids can inoculate caulimoviruses for several hours after acquisition and in the case of CaMV for up to 3 days depending on aphid species (Chalfant & Chapman, 1962). CaMV, at least, requires a virus-coded factor, which is not in the virus particles, for aphid transmission (Lung & Pirone, 1973; 1974). This transmission factor is probably a polypeptide of M. Wt 18,000 encoded by gene II of the viral DNA (Woolston et al., 1983; Armour et al., 1983). It co-sediments with the virus-induced inclusion bodies.
Ecology and Control
Caulimoviruses are not reported to be seed-transmitted or to be spread by contact. The world-wide distribution of CERV and DaMV, and probably that of CaMV, is mainly a result of dissemination of infected plant material.
Relations with Cells and Tissues
Caulimoviruses usually infect hosts systemically; they are found in most mesophyll, parenchyma and epidermal cells and sometimes in phloem sieve tubes and tracheids. Virus particles occur in spherical or ellipsoidal cytoplasmic inclusions, 5-20 µm in diameter, which lack a limiting membrane and are usually surrounded by numerous ribosomes (see review by Francki et al., 1985). In early stages of infection, the inclusions are small and scattered through the cytoplasm, though usually near the nuclei; in later stages the inclusions merge to form one or two per cell. The inclusion bodies consist of a finely granular matrix with several non-staining (electron-transparent) areas of varied size. Those of CaMV comprise mainly a virus-coded matrix protein of M. Wt 62,000-66,000 (Al Ani et al., 1980; Odell & Howell, 1980; Covey & Hull, 1981); however, Shepherd, Richins & Shalla (1980) reported the major matrix protein to be host-coded and of M. Wt 55,000. CaMV inclusion bodies also contain virus-specific DNA and RNA. The inclusion bodies of other caulimoviruses too contain protein the nature of which is unknown.
Virus particles are also sometimes found free in the cytoplasm and very occasionally in the nucleus (e.g. CERV: Lawson & Hearon, 1980) or in enlarged plasmodesmata (e.g. DaMV: Kitajima & Lauritis, 1969). Cell-wall thickening and protrusions frequently occur in infected cells (CERV: Descr. No. 182; DaMV: Kitajima & Lauritis, 1969; CaMV: Conti et al., 1972; MMV: Brunt & Kitajima, 1973).
Properties of Particles
Particles: Properties of caulimovirus particles are summarised in Table 1. When negatively stained in potassium phosphotungstate most have particle diameters of about 50 nm, frequently with an electron-dense centre. Neutron scattering analysis (Chauvin et al., 1979) showed that CaMV particles have a diameter of 49 nm and consist of a protein shell of 6.5 nm thickness, the DNA forming a layer on the inside of the shell; there is little or no protein or DNA in the particle centre.
Nucleic acid: The genomes of all caulimoviruses so far analysed are double-stranded DNA of 7.8-8.0 kbp (about 5 x 106 M. Wt) (Table 1); one isolate of CaMV with a deletion has only 7.6 kbp of DNA. The DNA of CaMV represents about 17% of the particle weight (Hull, Shepherd & Harvey, 1976) and has a Tm of 87.2°C in 0.15 M NaCl, 0.015 M Na citrate, a buoyant density in CsCl of 1.702 g/cm3 (Shepherd, Bruening & Wakeman, 1970) and a contour length of 2.31 µm (Shepherd & Wakeman, 1971) or 2.47 µm (Russell et al., 1971).
Coat protein: Gel electrophoresis of CaMV coat protein reveals several major bands with M. Wts (x 10-3) of approximately 65, 42, 37 and 35 (Tezuka & Taniguchi, 1972; Kelly, Cooper & Walkey, 1974; Brunt et al., 1975; Hull & Shepherd, 1976). These are probably degradation and/or aggregation products of a single protein of M. Wt 42,000 (Al Ani, Pfeiffer & Lebeurier, 1979) derived from a virus-coded (gene IV) product of M. Wt 57,000 (Franck et al., 1980). As well as being processed, CaMV coat protein is glycosylated (Hull & Shepherd, 1976; du Plessis & Smith, 1981) and phosphorylated (Hahn & Shepherd, 1980). MMV has a coat protein of M. Wt 32,000 (Brunt & Kitajima, 1973). There is no information on coat proteins of other caulimoviruses.
Other constituents: None reported. CaMV particles contain less than 0.1% fatty acid (Hull et al., 1976).
The DNA molecules of CaMV, CERV, DaMV, FMV, MMV and ThMV are found as both circular and linear forms, the circular forms having many different twisted conformations revealed by gel electrophoresis (Desc. No. 182; Hull & Howell, 1978; Hull & Donson, 1982; Donson & Hull, 1983; Richins & Shepherd, 1983). For CaMV the circular form only is infective (Hull & Shepherd, 1977). Caulimovirus DNA molecules are relaxed and have three or four discontinuities, one in one strand (the a- strand) and two or three in the other strand. Restriction endonuclease mapping shows that these discontinuities are at fixed positions (Hull & Howell, 1978; Volovitch, Drugeon & Yot, 1978; Hull & Donson, 1982; Donson & Hull, 1983; Richins & Shepherd, 1983). The 5'-end at each discontinuity of CaMV DNA is at a fixed nucleotide position (Hull et al., 1979) whereas the 3'-portion overlaps the 5'-end to a variable extent (Franck et al., 1980; Richards, Guilley & Jonard, 1981). The DNA molecules of three CaMV isolates have been sequenced, that of Cabb S being 8024 bp (Franck et al., 1980), that of CM-1841 being 8031 bp (Gardner et al., 1981) and that of D/H being 8016 bp (Balazs et al., 1982). The sequences show 6, or possibly 8, open reading frames (putative genes) on one strand, the other strand being non-coding.
Transcription of CaMV DNA occurs in the nucleus (Guilfoyle, 1980) from covalently closed DNA molecules in the form of mini-chromosomes (Olszewski, Hagen & Guilfoyle, 1982) most probably by RNA polymerase II (Guilfoyle, 1980); transcription takes place only from the a-strand (Howell & Hull, 1978; Hull et al., 1979). Two major polyadenylated transcripts are found, 19 S and 35 S. The 19 S RNA is transcribed from the part of the CaMV genome containing gene VI and is translated to give a protein of 62,000 M. Wt which is considered to be the matrix protein of the inclusion bodies (Odell & Howell, 1980; Al Ani et al., 1980; Covey & Hull, 1981; Xiong et al., 1982). No translation products have been reported from the 35 S RNA and it is not known how the proteins specified by genes I-V are produced. No information on transcription or translation has been reported for other caulimoviruses.
The 35 S RNA is a complete transcript of CaMV DNA and has a terminal repeat of 180 nucleotides (Covey, Lomonossoff & Hull, 1981; Dudley, Odell & Howell, 1982; Guilley et al., 1982). It is thought to be the template for the replication of virus DNA by a reverse transcription mechanism (Hull & Covey, 1983a, 1983c; Pfeiffer & Hohn, 1983). Unpackaged DNA molecules, of forms consistent with this replication mechanism, are found in infected leaves (Covey, Turner & Mulder, 1983; Hull & Covey, 1983b).
Serological inter-relationships have been reported between CaMV, CERV, DaMV and SVBV (Brunt, 1966; Brunt, 1971; Lawson & Civerolo, 1976; Morris et al., 1980); CaMV is also serologically related to HRLV (Richins & Shepherd, 1983). No serological relationship was found between MMV and CaMV, CERV or DaMV (Brunt & Kitajima, 1973) or between BRRV and CaMV (Kim et al., 1981). However care must be taken in the interpretation of serological data involving caulimoviruses because the coat protein of at least CaMV undergoes proteolysis (Al Ani et al., 1979; Hahn & Shepherd, 1980) and proteolysis can affect the serological reactivity of CaMV (du Plessis & von Wechmar, 1980). Nucleic acid hybridisation tests show that there is little or no homology between the DNA molecules of CaMV, CERV, DaMV, FMV, MMV and ThMV (Richins & Shepherd, 1983; J. Donson & R. Hull, unpublished observation); there is a greater degree of homology between the DNA molecules of CaMV and HRLV (Richins & Shepherd, 1983).
Features that place viruses as definitive members of the caulimovirus group (Table 1) include the induction of inclusion bodies, possession of isometric particles of about 50 nm diameter, and possession of a genome composed of circular double-stranded DNA of about 8 kbp which has a twisted conformation and several single-stranded discontinuities. Doubtful members are BRRV, which has two sedimenting components (Kim et al., 1981), and PVCV, which has smaller particles and some non-characteristic features in its inclusion bodies (Lesemann & Casper, 1973).
Affinities with Other Groups
Caulimoviruses are the only plant viruses known to contain double-stranded DNA. Possible very distant relationships to the vertebrate-infecting retroviruses are suggested by amino-acid homologies between the CaMV gene V product and the reverse transcriptases of retroviruses (Toh, Hayashida & Miyota, 1983).
References list for DPV: Caulimovirus group (295)
- Al Ani, Pfeiffer & Lebeurier, Virology 93: 188, 1979.
- Al Ani, Pfeiffer, Whitechurch, Lesot, Lebeurier & Hirth, Annls Virol. 131E: 33, 1980.
- Armour, Melcher, Pirone, Lyttle & Essenberg, Virology 129: 25, 1983.
- Balazs, Guilley, Jonard & Richards, Gene 19: 239, 1982.
- Brunt, Virology 28: 778, 1966.
- Brunt, Ann. appl. Biol. 67: 357, 1971.
- Brunt & Kitajima, Phytopath Z. 76: 265, 1973.
- Brunt, Barton, Tremaine & Stace-Smith, J. gen. Virol. 27: 101, 1975.
- Chalfant & Chapman, J. econ. Ent. 55: 584, 1962.
- Chauvin, Jacrot, Lebeurier & Hirth, Virology 96: 640, 1979.
- Conti, Vegetti, Bassi & Favali, Virology 49: 694, 1972.
- Covey & Hull, Virology 111: 463, 1981.
- Covey, Lomonossoff & Hull, Nucl. Acids Res. 9: 6735, 1981.
- Covey, Turner & Mulder, Nucl. Acids Res. 11: 251, 1983.
- Donson & Hull, J. gen. Virol. 64: 2281, 1983.
- Dudley, Odell & Howell, Virology 117: 19, 1982.
- du Plessis & Smith, Virology 109: 403, 1981.
- du Plessis & von Wechmar, Virology 107: 298, 1980.
- Franck, Guilley, Jonard, Richards & Hirth, Cell 21: 285, 1980.
- Francki, Milne & Hatta, An Atlas of Plant Viruses, Boca Raton: CRC Press, 2 vols, 1985.
- Gardner, Howarth, Hahn, Brown-Luedi, Shepherd & Messing, Nucl. Acids Res. 9: 2871, 1981.
- Guilfoyle, Virology 107: 71, 1980.
- Guilley, Dudley, Jonard, Balazs & Richards, Cell 30: 763, 1982.
- Hahn & Shepherd, Virology 107: 295, 1980.
- Hammond, Pl. Path. 30: 237, 1981.
- Hammond, Adv. Virus Res. 27: 103, 1982.
- Handley, Duffus & Shepherd, Phytopathology 72: 952, 1982.
- Howell & Hull, Virology 86: 468, 1978.
- Hull & Covey, Trends biochem. Sci. 8: 119, 1983a.
- Hull & Covey, Nucl. Acids Res. 11: 1881, 1983b.
- Hull & Covey, Sci. Prog., Oxford 68: 403, 1983c.
- Hull & Donson, J. gen. Virol. 60: 125, 1982.
- Hull & Howell, Virology 86: 482, 1978.
- Hull & Shepherd, Virology 70: 217, 1976.
- Hull & Shepherd, Virology 79: 216, 1977.
- Hull, Shepherd & Harvey, J. gen. Virol. 31: 93, 1976.
- Hull, Covey, Stanley & Davies, Nucl. Acids Res. 7: 669, 1979.
- Iwaki, Isogawa, Tsuzuki & Honda, Pl. Dis. 68: 1009, 1984.
- Kelly, Cooper & Walkey, Microbiol. 10: 239, 1974.
- Kennedy, Day & Eastop, A Conspectus of Aphids as Vectors of Plant Viruses, London: Commonwealth Institute of Entomology, 114 pp., 1962.
- Kim, Ramsdell, Gillett & Fulton, Phytopathology 71: 673, 1981.
- Kitajima & Costa, Bragantia 25: 211, 1966.
- Kitajima & Lauritis, Virology 37: 681, 1969.
- Lawson & Civerolo, Acta Hort. 59: 49, 1976.
- Lawson & Hearon, Phytopathology 70: 327, 1980.
- Lesemann & Casper, Phytopathology 63: 1118, 1973.
- Lin & Kitajima, Fitopatologia Brasileira 5: 419, 1980.
- Lung & Pirone, Phytopathology 63: 910, 1973.
- Lung & Pirone, Virology 60: 260, 1974.
- Morris, Mullin, Schlegel, Cole & Alosi, Phytopathology 70: 156, 1980.
- Odell & Howell, Virology 102: 349, 1980.
- Olszewski, Hagen & Guilfoyle, Cell 29: 395, 1982.
- Pfeiffer & Hohn, Cell 33: 781, 1983.
- Ragozzino, Annali Fac. Sci. agr. Univ. Napoli IV 8: 249, 1974.
- Richards, Guilley & Jonard, FEBS Lett. 134: 67, 1981.
- Richins & Shepherd, Virology 124: 208, 1983.
- Russell, Follett, Subak-Sharpe & Harrison, J. gen. Virol. 11: 129, 1971.
- Shepherd & Lawson, in Handbook of Plant Virus Infections and Comparative Diagnosis, p. 847, ed. Kurstak, Amsterdam: Elsevier/North-Holland, 1981.
- Shepherd & Wakeman, Phytopathology 61: 188, 1971.
- Shepherd, Bruening & Wakeman, Virology 41: 339, 1970.
- Shepherd, Richins & Shalla, Virology 102: 389, 1980.
- Tezuka & Taniguchi, Virology 48: 297, 1972.
- Toh, Hayashida & Miyota, Nature, Lond. 27: 827, 1983.
- Volovitch, Drugeon & Yot, Nucl. Acids Res. 5: 2913, 1978.
- Woolston, Covey, Penswick & Davies, Gene 23: 15, 1983.
- Xiong, Balazs, Lebeurier, Hindelang, Stoeckel & Porte, J. gen. Virol. 61: 75, 1982.