13
June 1970
Family: Closteroviridae
Genus: Closterovirus
Species: Beet yellows virus
Acronym: BYV

There is a more recent description of this virus: DPV 377

Beet yellows virus

G. E. Russell
Plant Breeding Institute, Trumpington, Cambridge, England

Contents

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

Introduction

Described by Roland (1936), Watson (1942) and Hull (1950).

Selected synonyms:

Virus de la jaunisse de la betterave (Rev. appl. Mycol. 15: 548)
Beta virus 4 (Rev. appl. Mycol. 36: 308)
Corium betae (Rev. appl. Mycol. 19: 229)

A virus with flexuous filamentous particles c. 1250 nm long. Transmitted by many species of aphid in the semi-persistent manner but by sap inoculation only with difficulty. Host range moderate, mainly in the Chenopodiaceae. Widely distributed throughout the beet-growing areas of the world.

Main Diseases

Causes a yellows disease in Beta vulgaris (sugar beet, red beet, spinach beet, etc.) and in Spinacia oleracea (spinach).

Geographical Distribution

World-wide in major sugar beet growing areas.

Host Range and Symptomatology

Host range is moderate, mainly in the Chenopodiaceae; species in at least ten dicotyledonous families have been infected experimentally (Bennett, 1960). Transmitted readily by aphid inoculation, with difficulty by manual inoculation of sap, for example to the following species:

Diagnostic species

Beta vulgaris (sugar beet). Young leaves of glasshouse plants often show vein-clearing and ‘vein-etch’ (Fig.1). Older leaves of field and glasshouse beet become yellow, thickened and brittle and usually have numerous small red or brown necrotic spots (Fig.2).

Chenopodium foliosum or C. capitatum. Acute stunting, distortion and vein-clearing in young leaves (Fig.3), and usually premature death.

Claytonia perfoliata. Plants inoculated by aphids show systemic red spots and chlorosis in older leaves (Fig.4). Manually inoculated plants develop red necrotic lesions in inoculated leaves but do not become infected systemically (Russell, 1963).

Propagation species

Sugar beet, Claytonia perfoliata or Tetragonia expansa are suitable for maintaining cultures.

Assay species

Claytonia perfoliata is a good host for sap inoculation tests and also for testing aphids.

Sugar beet and Chenopodium foliosum are satisfactory alternatives although in these the virus may become systemic even after sap inoculation.

Strains

Many minor variants have been isolated from local lesions, producing symptoms in sugar beet ranging from very mild yellowing to very severe vein-etch and leaf necrosis. All are apparently serologically related and there is usually complete cross-protection between them (Russell, 1964), Bennett (1960), however, described some strains which do not cross protect.

Transmission by Vectors

Transmissible by more than 22 species of aphids (Kennedy, Day & Eastop, 1962) but Myzus persicae and Aphis fabae are the principal vectors in the field. All instars transmit but adults are the most efficient. Transmission is of the semi-persistent type (Watson, 1946; Sylvester, 1956), the virus being retained by the vector for up to 3 days, with a half-life of about 8 hr. For optimum transmission, acquisition feeds of more than 12 hr and test feeds of at least 6 hr are necessary. Probably no latent period. Not transmitted to progeny of vectors. Vectors do not retain virus after moulting (Watson, 1960).

Transmission through Seed

Early reports of seed transmission have not been confirmed.

Transmission by Dodder

Several species can transmit (Fuchs & Beiss, 1954). Aphids can acquire virus from some non-transmitting species of dodder growing on infected plants (Bennett, 1960).

Serology

The virus is weakly immunogenic. Antisera may be prepared by intravenous, intramuscular or intraperitoneal injections of clarified sap from infected plants; sap from Claytonia perfoliata is particularly suitable. Tube-precipitin or slide-agglutination tests, using clarified sap, are satisfactory for routine diagnosis and crude quantitative assays.

Relationships

No evidence of serological relationship to any other virus (Brandes & Bercks, 1965). Resembles citrus tristeza, festuca necrosis, apple chlorotic leaf spot, apple stem-pitting and citrus tatter-leaf viruses in several features, particularly particle morphology, symptomatology and difficulty of sap inoculation (Gibbs, 1969).

Stability in Sap

Thermal inactivation point (10 min) in sap is about 55°C; dilution end point is up to 10-4 depending on host plant used. Infectivity is retained in frozen sap for more than a year but rarely for more than 1 day at 20°C.

Purification

The virus is very unstable. Partial purification from clarified sap has been achieved by differential centrifugation. The virus forms a single light-scattering zone when centrifuged in sucrose density gradients (Mundry, 1958).

Properties of Particles

Unknown.

Particle Structure

Flexuous filamentous particles about 1250 nm long and 10 nm in diameter with sub-units arranged around a hollow core (Horne, Russell & Trim, 1959) in a helix of pitch between 3.0 and 3.4 nm (Varma, Gibbs, Woods & Finch, 1968). Good contrast achieved by mixing 2% phosphotungstate with virus in clarified sap (Fig.5).

Particle Composition

Unknown.

Relations with Cells and Tissues

Particularly associated with degeneration of phloem tissues. Arrays of virus particles have been found in chloroplasts (Cronshaw, Hoefert & Esau, 1966).

Notes

Beet yellows virus often occurs in beet together with beet mild yellowing or beet western yellows viruses, which, however, are transmitted by aphids in the persistent manner. They also differ from beet yellows virus in symptomatology, host range, particle morphology and in serological tests (Russell, 1968; Duffus, 1964; Gold & Duffus, 1967).

References

  1. Bennett, Tech. Bull. U.S. Dep. Agric. 1218, 63 pp., 1960.
  2. Brandes & Bercks, Adv. Virus Res. 11: 1, 1965.
  3. Cronshaw, Hoefert & Esau, J. Cell Biol. 31: 429, 1966.
  4. Duffus, Phytopathology 54: 736, 1964.
  5. Fuchs & Beiss, Naturwissenschaften 41: 506, 1954.
  6. Gibbs, Adv. Virus Res. 14: 288, 1969.
  7. Gold & Duffus, Virology 31: 308, 1967.
  8. Horne, Russell & Trim, J. molec. Biol. 1: 234, 1959.
  9. Hull, Bull. Minist. Agric. Fish. Fd Lond. 142, 53 pp., 1950.
  10. Kennedy, Day & Eastop, A conspectus of aphids as vectors of plant viruses,London, Commonwealth Institute of Entomology, 1962.
  11. Mundry, Z. Naturf. Ser. B. 13: 19, 1958.
  12. Roland, Sucr. belge 55: 213, 1936.
  13. Russell, Nature, Lond. 197: 623, 1963.
  14. Russell, Ann. appl. Biol. 53: 377, 1964.
  15. Russell, Br. Sug. Beet Rev. 37: 77, 1968.
  16. Sylvester, J. Am. Soc. Sug. Beet Technol. 9: 56, 1956.
  17. Varma, Gibbs, Woods & Finch, J. gen. Virol. 2: 107, 1968.
  18. Watson, Ann. appl. Biol. 29: 358, 1942.
  19. Watson, Proc. R. Soc. B, 133: 200, 1946.
  20. Watson, Rep. 7th Commonwealth Entom. Conf. London: 157, 1960.

Acknowledgements

Photographs: courtesy of Plant Breeding Institute, Cambridge; Fig.5 courtesy of Rothamsted Experimental Station.


Figure 1

Leaves from glasshouse-grown sugar beet seedlings: (left) virus-free, (right) infected.

Figure 2

Mature leaf of field-infected sugar beet, showing chlorosis and necrotic spots which are usually more numerous near the leaf tip. Such leaves are invariably thickened and brittle.

Figure 3

Chenopodium foliosum seedlings: (left) virus-free, (right) infected, showing vein-clearing and distortion in young leaves.

Figure 4

Leaves of Claytonia perfoliata: (left) virus-free, (right) systemically infected.

Figure 5

Electron micrograph of part of a filament showing periodicity along axis. Bar represents 100 nm.