Details of DPV and References

DPV NO: 112 July 1973

Family: Betaflexiviridae
Genus: Carlavirus
Species: Pea streak virus | Acronym: PeSV

Pea streak virus

L. Bos Institute of Phytopathological Research, Wageningen, The Netherlands

Contents

Introduction

Described by Zaumeyer (1938), Hagedorn & Walker (1949) and Wetter, Quantz & Brandes (1962).

Selected synonyms

Marmor iners (Rev. appl. Mycol. 28: 514)
Pea streak virus 1 (Rev. appl. Mycol. 17: 220)
Sweet clover virus (Steinkleevirus) (Rev. appl. Mycol. 36: 532)
Wisconsin pea streak virus (Rev. appl. Mycol. 29: 132)

An RNA-containing virus with straight to slightly curved filamentous particles c. 620 x 12 nm. Easily sap-transmitted to many species in the Papilionaceae and to some in other families, often causing latent infection. Certain isolates are readily aphid-transmitted, others poorly or not at all.

Main Diseases

Causes severe necrotic streaking of pea stems and petioles often with veinal necrosis; other symptoms are flaccidity of leaves, malformation and chlorosis of apical foliage, wilting of plant tips and plant death (Fig. 1). Pods may be spotted, pitted and distorted; those forming when infection takes place become purple and do not develop seeds. In pea no immunity seems to exist (Hagedorn, 1968). In Minnesota and Wisconsin (Hanson & Hagedorn, 1961; Stuteville & Hanson, 1965a) and in Canada (Pratt, 1968) clovers (especially red clover) are commonly infected, often without symptoms. In red clover no immunity was found (Stuteville & Hanson, 1964b). Natural infection of white sweet clover (Steinkleevirus) was reported only once (Quantz & Brandes, 1957).

Geographical Distribution

Prevalent in pea growing areas in USA (Wisconsin, Idaho, Washington). Occurs in clovers in Canada and USA; reported once in sweet clover in West Germany.

Host Range and Symptomatology

Natural hosts are peas and clovers. Experimental hosts belong mainly to the Papilionaceae (legumes) and several produce no symptoms (Wetter et al., 1962). Phaseolus vulgaris is not susceptible to most isolates but was infected by the New Zealand pea streak virus (Chamberlain, 1939). This isolate and the German Steinkleevirus caused local infection in Cucumis sativus. The Steinkleevirus induced local infection in Chenopodium quinoa. The Wisconsin strain was reported to infect tomato (Kim & Hagedorn, 1959).

Diagnostic species
Chenopodium amaranticolor. With the Wisconsin pea streak virus many necrotic local lesions (Fig. 2) develop after 4 days at 28°C or 7 days at 16°C, each surrounded by a chlorotic halo which becomes broader with increasing temperature. Lesions are more numerous at 16°C than at 28°C (Rosenkranz & Hagedorn, 1964).

Gomphrena globosa. White sunken local lesions 0.5-1 mm in diameter develop 2-3 days after inoculation, later surrounded by chlorotic reddening borders; such lesions can be easily distinguished from those induced by alfalfa mosaic or red clover vein mosaic viruses, which develop 6 days later (Stuteville & Hanson, 1965b).

Pisum sativum (pea). Many varieties react with typical necrotic streaking of stems and petioles, and malformation and chlorosis of top leaves. In the greenhouse, symptoms are less severe and mainly consist of progressive wilting; stem streaking is more typical at lower temperatures (16°C) (Hagedorn & Walker, 1949).

Vicia faba (broad bean). Necrotic local lesions develop in 6-8 days, followed by necrotic streaks on stems, and rosetting and malformation of plant tips; often plants die back gradually from the growing point. In the cultivar ‘Compacta’ the Wisconsin strain induces numerous chlorotic lesions after 4 days, later developing into necrotic rings with a dry centre (Fig. 3). Lesions induced by the RK31 and P42 strains of red clover vein mosaic virus appear at least 5 days later and are less reliable (Bos et al., 1972).

Propagation species
Pisum sativum. With the Wisconsin strain, concentration was highest at 24°C in systemically infected leaves 20-35 days after the plants were inoculated. Virus concentration was also high in stems and roots (Rosenkranz & Hagedorn, 1967).

Assay species
Chenopodium amaranticolor, Gomphrena globosa and Vicia faba are useful local lesion hosts. Standardized conditions for quantitative assay of the Wisconsin strain in C. amaranticolor were given by Rosenkranz & Hagedorn (1964).

Strains

The variants described differ little in host range and symptomatology. The original isolates of the incompletely described pea streak virus (Zaumeyer, 1938) and New Zealand pea streak virus (Chamberlain, 1939), are no longer available for comparison.

Wisconsin strain of Hagedorn & Walker (1949) is mainly distinguished by its long survival in vitro (50-60 days) and its poor transmission by Acyrthosiphon pisum.

Idaho strain of Kim & Hagedorn (1959) resembles the Wisconsin strain in many respects and both viruses react strongly with each other’s antisera, but its longevity in vitro is only 4-7 days and it is readily transmitted by A. pisum. Perhaps identical to the Idaho strain of Zaumeyer & Patino (1959).

Sweet clover strain of Quantz & Brandes (1957) is serologically and in many other properties indistinguishable from the Idaho strain, but has occasionally been recovered from experimentally infected Phaseolus bean (Wetter et al., 1962).

Transmission by Vectors

The Idaho strain was easily transmitted by the pea aphid (Acyrthosiphon pisum) after acquisition feeding periods varying from 15 min to 30 hr. Under similar conditions the Wisconsin strain was not transmitted (Kim & Hagedorn, 1959). In a more extensive trial A. pisum transmitted the Wisconsin strain to 0.32% and 3.27% of the plants after acquisition feeding times of 15 sec and 24 hr respectively (Skotland & Hagedorn, 1954). When allowed only single probes, aphids transmitted the virus to at least 5 sequential test plants; after feeding for 15 min on the first test plant 4% of the aphids still transmitted to other test plants (Hampton & Sylvester, 1969).

Transmission through Seed

No reports; not seed-transmitted in red clover (Stuteville & Hanson, 1964a).

Transmission by Dodder

Not reported.

Serology

The virus is strongly immunogenic. Highest titres (1/16,384) were obtained by injecting partially purified virus after removal of normal proteins with ‘healthy’ antiserum (Wetter et al., 1962). Tube precipitin tests have been used most often but microprecipitin tests under paraffin oil are also satisfactory (Bos, Maat & Markov, 1972).

Relationships

Serologically the two American strains of the virus and the German sweet clover strain are closely related. They differ considerably serologically and in particle length from strains of red clover vein mosaic virus, including the P42 strain of Zaumeyer, Goth & Ford (1964), which induces severe streak symptoms in pea (Wetter et al., 1962; Bos et al., 1972). The Minnesota (MS) pea streak virus, described by Kim & Hagedorn (1959) resembles pea streak virus in various ways but did not react with antisera prepared against the Wisconsin and Idaho strains, nor did these strains react with antiserum to the Minnesota pea streak virus.

Bos et al. (1972) found that, in pea, the Wisconsin strain of pea streak virus gave weak protection against normal (RK31) and pea streak (P42) strains of the red clover vein mosaic virus. In host range, symptoms and properties in expressed sap, the virus resembles the broad bean local-lesion virus from red clover, incompletely characterized by Pierce (1935).

Stability in Sap

In pea sap, the thermal inactivation point (10 min) is usually above 60°C and sometimes 78-80°C, dilution end-point is up to 10-6-10-7, and infectivity persists from 2-7 days, but up to 50-60 days for the Wisconsin strain.

Purification

Wetter (1960): Express sap from infected pea plants and add ascorbic acid to 0.2% (w/v) and sodium sulphite to 0.2% (w/v). Filter and shake filtrate with equal volume of ether. Centrifuge and shake the clarified aqueous phase with an equal volume of carbon tetrachloride. Sediment and clarify by two cycles of high and low speed centrifugation, resuspending the pellets in 0.01 M phosphate buffer. Density gradient centrifugation can be used for further purification.

Bos et al. (1972): Homogenize 200 g of infected pea plants in 300-400 ml 0.18 M phosphate-citric acid buffer (pH 7, containing 0.1% thioglycollic acid), 100 ml ether and 100 ml carbon tetrachloride. After one low speed centrifugation, give two cycles of differential centrifugation and resuspend in the above buffer. Purify further by sucrose density gradient centrifugation, e.g. in a zonal rotor and concentrate by ultracentrifugation.

Properties of Particles

Sedimentation coefficient (s20) at infinite dilution: 160 S (Bos et al., 1972), 136-137 S (Rosenkranz & Hagedorn, 1967; not corrected for concentration and impurities).

A260/A280: 1.33-1.35 (calculated after Kim & Hagedorn, 1959).

Particle Structure

Particles are straight or slightly curved filaments (Fig. 4), with modal lengths of c. 619 nm (Wetter et al., 1962) or 630 nm (Bos et al., 1972) after negative staining, with tobacco mosaic virus as an internal standard. For comparison the same authors found 654 and 670 nm, respectively, for red clover vein mosaic virus.

Particle Composition

15.5% of the particle weight is nitrogen and 0.53% is phosphorus. RNA is 5.4% of particle weight (Rosenkranz & Hagedorn, 1967).

Relations with Cells and Tissues

In pea epidermal cells extensive parts of the cytoplasm are often stainable with phloxine and sometimes contain well-defined granular and vacuolated inclusion bodies (Fig. 5). Negatively stained pea leaf sap preparations contain large amounts of non-aggregated particles often attached to cell organelles (Fig. 4). In ultrathin sections, particles occur separately, or more frequently in bundles attached to membranes, e.g. around vacuoles (Fig. 6) (Bos & Rubio-Huertos, 1972).

Notes

The virus closely resembles red clover vein mosaic virus in particle morphology, host range and symptoms in most hosts (but see Diagnostic Hosts). Serologically, however, the two viruses are only distantly related and they can be easily distinguished by their differing particle lengths even in mixed preparations (Wetter et al., 1962; Bos et al., 1972). Certain strains of red clover vein mosaic virus cause more severe necrotic streaking than pea streak virus itself, e.g. strain P42 of Zaumeyer et al. (1964).


Many other viruses are known to cause necrotic streak diseases in pea, viz.: alfalfa mosaic, bean yellow mosaic, beet mosaic, broad bean wilt, cucumber mosaic, lettuce mosaic, pea early-browning, pea necrosis, tobacco ringspot, tobacco streak, tomato spotted wilt and white clover mosaic viruses. They are difficult to distinguish from each other symptomatologically, but can usually be easily differentiated from true pea streak virus by their ability to infect some or several non-legumes and by their different particle morphology.

Figures

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Pea plant with symptoms of Wisconsin pea streak as seen in the field. (After Hagedorn & Walker, 1954.)

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Local lesions in Chenopodium amaranticolor 7 days after inoculation. (After Rosenkranz & Hagerdorn, 1964.)

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Local lesions in Vicia faba 'Compacta'. (After Bos et al., 1972.)

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Virus particles (left) after negative staining and (right) after shadow casting; bars represent 500 nm. (After Bos & Rubio-Huertos.)

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Inclusions (I) in pea leaf epidermis; N= nucleus. Bar represents 10 µm. (After Bos & Rubio-Huertos.)

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Virus aggregates in ultrathin section of pea leaf tissue; bar represents 500 nm. (After Bos & Rubio-Huertos, 1972.)

References list for DPV: Pea streak virus (112)

  1. Bos, Maat & Markov, Neth. J. Pl. Path. 78: 125, 1972.
  2. Bos & Rubio-Huertos, Neth. J. Pl. Path. 78: 247, 1972.
  3. Chamberlain, N. Z. Jl Sci. Technol. 20: 365A, 1939.
  4. Hagedorn, Pl. Dis. Reptr 52: 160, 1968.
  5. Hagedorn & Walker, Phytopathology 39: 837, 1949.
  6. Hagedorn & Walker, Res. Bull. agric. Exp. Stn Univ. Wis. 185: 32 pp., 1954.
  7. Hampton & Sylvester, Phytopathology 59: 1663, 1969.
  8. Hanson & Hagedorn, Agron. J. 53: 63, 1961.
  9. Kim & Hagedorn, Phytopathology 49: 656, 1959.
  10. Pierce, J. agric. Res. 51: 1017, 1935.
  11. Pratt, Can. Pl. Dis. Surv. 48: 87, 1968.
  12. Quantz & Brandes, NachrBl. dt. PflSchutzdienst., Stuttg. 9: 6, 1957.
  13. Rosenkranz & Hagedorn, Phytopathology 54: 807, 1964.
  14. Rosenkranz & Hagedorn, Phytopathology 57: 551, 1967.
  15. Skotland & Hagedorn, Phytopathology 44: 569, 1954.
  16. Stuteville & Hanson, Pl. Dis. Reptr 48: 270, 1964a.
  17. Stuteville & Hanson, Crop Sci. 4: 631, 1964b.
  18. Stuteville & Hanson, Crop Sci. 5: 59, 1965a.
  19. Stuteville & Hanson, Phytopathology 55: 336, 1965b.
  20. Wetter, Arch. Mikrobiol. 37: 278, 1960.
  21. Wetter, Quantz & Brandes, Phytopath. Z. 44: 151, 1962.
  22. Zaumeyer, J. agric. Res. 56: 747, 1938.
  23. Zaumeyer, Goth & Ford, Pl. Dis. Reptr 48: 494, 1964.
  24. Zaumeyer & Patino, Pl. Dis. Reptr 43: 698, 1959.