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Selected text for Sweetpotato chlorotic stunt crinivirus
Preferred name
Sweetpotato chlorotic stunt crinivirus
Taxonomic position
Genus: Crinivirus
Family: Closteroviridae
Class: Virus
Other names used
Sweet potato sunken vein virus
SPVD-associated closterovirus (SPVD-AC)
Whitefly-borne component
Whitefly transmitted agent
Acronym: SPCSV
Common names
English: Sweetpotato chlorotic stunt virus
Spanish: Enanismo clorótico del camote
Notes on taxonomy and nomenclature
SPCSV is the first name given to the whitefly-transmitted agent of the SPVD from Nigeria
(Schaefers and Terry, 1976) by the symptomatology it induced in Ipomoea setosa. SPCSV is
considered a synonim of sweetpotato sunken vein virus (SPSVV) named by Cohen et al. (1992).
Later, Gibson et al. (1998) reinstated the name of SPCSV for the virus found in the complex
named sweetpotato virus disease (SPVD).
SPCSV is a member of the crinivirus genus in the Family Closteroviridae.
Host range
Ipomoea batatas, I. hederacea, I. trichiocarpa, I. tricolor,I. Nil, I. Setosa, I. Trifida Nicotiana
benthamiana, and N. clevelandii have been shown to be susceptible to the virus.
Affected plant stage
Vegetative growing stage
Affected plant parts
Leaves
List of hosts
Primary host is I. batatas (sweetpotato). No secondary hosts have been reported.
Geographic distribution
SPCSV has been reported from Africa (Schaefers and Terry, 1976) and Israel (Cohen et al.,
1992) . In South America has been reported occurring as a complex in the chlorotic dwarf disease
from Argentina (Di Feo et al., in press) and found in Peru and Brazil though no published reports
are available.
Biology and Ecology
SPCSV is transmitted by the white fly Bemisia tabaci , in a semi-persistent manner. The virus is
not transmitted by mechanical inoculation nor by contact between plants. It is transmitted by
grafting.
Because the virus infects sweetpotato plants systemically, it is disseminated in infected
vegetatively-produced propagules (stem cuttings and roots). Plants grown from such propagules
are primary sources of infection, especially if they occur as volunteers.
Seedborne aspects
There is no evidence that SPCSV is seedborne.
Economic impact
By itself, SPCSV may cause only small yield losses in the first year but up to 30% in the second
year. However, in combination with SPFMV causes SPVD, a severe disease associated with
almost complete yield loss (Milgram et al., 1996; Hahn, 1979).
Symptoms- Description
The symptoms reported for SPCSV vary geographically; in East Africa, the disease may cause
color changes (purpling or yellowing) of lower or middle leaves (Gibson et al., 1998) depending
on the variety. Elsewhere, symptoms include mild vein yellowing, some sunken secondary veins
on adaxial leaf surfaces, and swollen veins on abaxial surfaces (Cohen et al., 1992). The virus
may also occur without producing noticeable symptoms.
SPCSV is primarily important when occurs together with SPFMV to cause the SPVD.
Morphology
The virus has flexuous, filamentous particles of 850-950 nm long with a coat protein of Mr 25-34
KD.
West (and from other countries) and East African strains are serologically distinct (Gibson et al.,
1998; Hoyer et al., 1996; Vetten, 1996)
Diagnostic methods
Indicator hosts
SPCSV can be transmitted by Bemisia tabaci or grafting to:
Ipomoea setosa – mild chlorosis/mosaic and/or severe stunting of the plant and small brittle
leaves. An inward of the leaves can also be observed (Winter et al., 1992).
I. nil – chlorosis and epinasty in new leaves followed by severe stunting and dwarfing of entire
leaf. Older leaves became bronze colored and brittle (Larsen et al., 1991).
Serological and Molecular Techniques
The virus can be detected by ISEM and ELISA using monoclonal and polyclonal antibodies.
Probes and primers for its detection by NASH and PCR had been developed. Analysis of dsRNA
can also be used (Abad et al., 1992; Winter et al., 1992).
Phytosanitary risk
Risk criteria
Category
Economic importance
high
Distribution
Worldwide
Seedborne incidence
No
Seed transmitted
No
Seed treatmemnt
None
Vector transmission
high
Transmission in planting materials high
Overall risk
high
Control
SPCSV is perpetuated through cropping cycles via infected cuttings. SPCSV is generally
identified in combination with SPFMV causing the severe disease SPVD.
The main measure to control SPCSV is avoidance of diseased plants as sources of planting
material, sanitation, and use of resistant or tolerant varieties (Gibson et al., 1997).
REFERENCES
Abad JA, French RD, and Moyer JW, 1992. Double stranded (ds) RNA analysis of the whitefly
component of the sweet potato virus disease (SPVD-WF) of sweet potato. Phytopathology, 82:
1170.
Cohen J, Franck A, Vetten HJ, Lesemann DE, and Loebenstein G, 1992. Purification and
properties of closterovirus-like particles associated with a whitefly-transmitted disease of sweet
potato. Annals Applied of Biology, 121: 257-268.
Di Feo L, Nome SF, Biderbost E, Fuentes S, and Salazar LF, 1999. Etiology of sweet potato
chlorotic dwarf disease in Argentina. Plant Disease (in press).
Gibson RW, Kaitisha GC, Randrianaivoarivony JM, and Vetten HJ, 1998. Identification of the
East African strain of sweet potato chlorotic stunt virus as a major component of sweet potato
virus disease in Southern Africa. Plant Disease, 82: 1063.
Gibson RW., Mwanga ROM, Kasule S, Mpembe I, and Carey EE, 1997. Apparent absence of
viruses in most symptomless field-grown sweet potato in Uganda. Annals Apply of Biology, 130:
481-490.
Hahn, S.K. 1979. Effects of viruses (SPVD) on growth and yield of sweetpotato. Expl. Agr. 15:
253-256.
Hoyer U, Maiss E, Jelkmann W, Lesemann DE, and Vetten HJ, 1996. Identification of the coat
protein gene of a sweet potato sunken vein closterovirus isolate from Kenya and evidence for e
serological reationship among geographically diverse closterovirus isolates from sweet potato.
Phytopathology, 86: 744-750.
Larsen RC, Laakso M, and Moyer JW, 1991. Isolation and vector relations of a whiteflytransmitted component of the sweet potato virus disease (SPVD) complex from Nigeria.
Phytopathology, 81: 1157.
Milgram M., Cohen J., and Loebenstein G, 1996. Effects of sweet potato feathery mottle virus
and sweet potato sunken vein virus on sweet potato yields and rates of reinfection of virus-free
planting material in Israel. Phytoparasitica 24: 189-193
Schaefers GA, and Terry ER, 1976. Insect transmission of sweet potato disease agents in Nigeria.
Phytopathology, 66: 642-645.
Vetten HJ, 1996. Serodiagnosis of sweet potato viruses: potencial and limitations. In: Procedings
of the Regional Sweetpotato Workshop held at Libreville, Gabon, January 9-13, 1996. CTA,
Wageningen. Pages 27-32.
Winter, S., Purac, A., Leggett, F., Frison, E.A., Rossel, H.W., and Hamilton, R.I. (1992). Partial
characterization and molecular cloning of a closterovirus from sweet potato infected with the
sweet potato virus disease complex from Nigeria. Phytopathology, 82: 869-875.