Details of DPV and References
DPV NO: 114 July 1973
Species: Hydrangea ringspot virus | Acronym: HdRSV
Hydrangea ringspot virus
Renate Koenig Biologische Bundesanstalt für Land- und Forstwirtschaft, Braunschweig, Germany
- Main Diseases
- Geographical Distribution
- Host Range and Symptomatology
- Transmission by Vectors
- Transmission through Seed
- Transmission by Grafting
- Transmission by Dodder
- Nucleic Acid Hybridization
- Stability in Sap
- Properties of Particles
- Particle Structure
- Particle Composition
- Properties of Infective Nucleic Acid
- Molecular Structure
- Genome Properties
- Relations with Cells and Tissues
- Ecology and Control
- Described by
Brierley (1954) and
Brierley & Lorentz (1957).
A virus with filamentous particles of normal length c. 490 nm. Readily transmitted by inoculation of sap; no vector known. World-wide distribution.
Many naturally infected Hydrangea macrophylla plants carry the virus without showing conspicuous symptoms. Crinkling, rolling and asymmetry of leaves (Fig. 1), decrease in number of florets per inflorescence, severe dwarfing and running out of hydrangea varieties have all been attributed to the presence of the virus. Experimentally infected hydrangeas may develop chlorotic or brown spots or rings on the leaves and may show distortion and buckling of the leaves several months after inoculation (Brierley & Lorentz, 1957; Hollings, 1958). Symptom expression probably depends on variety and environmental conditions.
Reported from USA, Europe and New Zealand. Probably world-wide in cultivated Hydrangea macrophylla.
Host Range and Symptomatology
Hydrangea macrophylla seems to be the only natural host. Experimentally, the virus causes infections in more than 20 species in 12 dicotyledonous families. It infects Primula malacoides systemically (Hollings, 1958), often without inducing symptoms.
- Gomphrena globosa.Local necrotic dots within 3-5 days, later enlarging and developing red margins (Fig. 4).
- Chenopodium quinoa. Local chlorotic spots within 5-7 days
(Fig. 2) sometimes
becoming bright yellow or necrotic or developing into chlorotic ringspots.
- Chenopodium amaranticolor. Local chlorotic dots with a central necrotic speck within 5-7 days.
- Primula malacoides.Naturally infected hydrangeas can also be used as a source of virus for purification.
- Gomphrena globosais the most sensitive indicator plant. Chenopodium quinoa and C. amaranticolor may also be used.
Minor variants can be distinguished on the basis of serology (Hollings, 1958; Belli & Belli, 1967) and symptom expression on Chenopodium quinoa (Koenig, 1970).
Transmission by Vectors
No vector known. Attempts to transmit the virus by the aphids Myzus persicae and Macrosiphum euphorbiae failed (Hollings, 1958).
Transmission through Seed
Not found (Brierley & Lorentz, 1957).
Transmission by Dodder
Apparently not tested.
The virus is strongly immunogenic, forming flagellar precipitates in tube or slide precipitin tests.
Particle morphology and physical properties place the virus in the potexvirus group (Brandes & Bercks, 1965). It is distantly serologically related to potato X, cactus X, white clover mosaic and clover yellow mosaic viruses.
Stability in Sap
In sap from hydrangea, the thermal inactivation point (10 min) is between 70 and 75°C, the dilution end-point is about 10-5 and infectivity is retained at room temperature for 2-3 weeks (Brierley & Lorentz, 1957; Hollings, 1958).
1. Mince 100 g hydrangea leaves with 20 ml 0.5 M borate buffer pH 7.8, add 0.2 g sodium sulphite and 0.2 g ascorbic acid and centrifuge expressed sap at low speed. Add 1 volume 0.1% silver nitrate to 6 volumes of the supernatant fluid, stir for 10 min and leave at room temperature for several hours. Centrifuge at low speed, add 1 volume of 20% polyethylene glycol 6000 in 0.5 M borate buffer, pH 7.8, to 4 volumes of the supernatant fluid, leave at 4°C for several hours. Centrifuge at low speed, resuspend the pellets in 15 ml of 0.5 M borate buffer containing 0.5 M urea and 0.1% 2-mercaptoethanol. Subject the virus to 1 or 2 cycles of differential centrifugation (R. Koenig, unpublished).
2. The ether-carbon tetrachloride method of Wetter (1960) can be used with extracts from infected Primula malacoides (Bercks & Brandes, 1961).
Properties of Particles
Electrophoretic mobility: -3.9 x 10-5 cm2 sec-1 volt-1 in 0.05 M sodium phosphate buffer at pH 7.0 (Sisler et al., 1957).
Absorbance at 260 nm (1 mg/ml, 1 cm light path): 3.08 (calculated from Sisler et al., 1957).
A260/A280: 1.22 (calculated from Sisler et al., 1957).
Particles are flexuous filaments (Fig. 3) with normal length c. 490 nm (Bercks & Brandes, 1961).
Nucleic acid: Probably single-stranded RNA for which a M. Wt of 2.5 x 106 is found by polyacrylamide gel electrophoresis (R. Koenig, unpublished).
Protein: SDS-polyacrylamide gel electrophoresis yields two bands corresponding to M. Wt of 1.9 and 2.2 x 104. Thin layer gel chromatography with Sephadex G 200 in the presence of 6 M guanidine hydrochloride and 0.1% 2-mercaptoethanol yields a single spot corresponding to a M. Wt of about 2.4 x 104 (R. Koenig, unpublished). As with the proteins of other potexviruses (Koenig, 1972) the meaning of multiple band formation in SDS-polyacrylamide gel electrophoresis is still unclear.
Relations with Cells and Tissues
No specific inclusions are seen in hydrangea, but chloroplasts are often clumped together. Epidermal hair cells of infected Primula malacoides often contain oval or elongated vacuolate bodies ranging from 13 x 32 to 11.5 x 50 µm. These inclusions stain intensely with 0.5% phloxine and sometimes contain discrete granules (Hollings, 1958).
Hydrangea ringspot virus can be differentiated from other viruses infecting Hydrangea macrophylla (i.e. tomato ringspot, tobacco ringspot, tobacco necrosis, cucumber mosaic and alfalfa mosaic viruses) by its inability to infect tobacco and other solanaceous hosts (but see Dunez, 1963) and by its elongated shape.
Fig. 1 courtesy of Dr M. Hollings, Littlehampton; Fig. 3 courtesy of Dr D. Lesemann, Braunschweig
References list for DPV: Hydrangea ringspot virus (114)
- Belli & Belli, Riv. Patol. veg., Pavia, Ser. IV, 3: 163, 1967.
- Bercks & Brandes, Phytopath. Z. 42: 45, 1961.
- Brandes & Bercks, Adv. Virus Res. 11: 1, 1965.
- Brierley, Phytopathology 44: 696, 1954.
- Brierley & Lorentz, Phytopathology 47: 39, 1957.
- Dunez, Annls. Épiphyt. 14: 103, 1963.
- Hollings, J. hort. Sci. 33: 275, 1958.
- Koenig, NachrBl. dt. PflSchutzdienst., Stuttg. 22: 34, 1970.
- Koenig, Virology 50: 263, 1972.
- Sisler, Chang, Reagan & Brierley, Phytopathology 47: 491, 1957.
- Wetter, Arch. Mikrobiol. 37: 278, 1960.