Sweetpotato chlorotic stunt virus

Taxonomy

Possibly the most damaging virus infecting sweetpotato and the most damaging pathogen of sweetpotato in Africa. By itself, SPCSV causes some yield loss, but its presence breaks resistance in sweetpotato to sweetpotato feathery mottle virus (SPFMV) and the combined infection causes the very severe disease, sweetpotato virus disease (SPVD).

Tropics worldwide: particularly prevalent in sub-Saharan Africa but recent reports of damage in South America.

By itself, infection by SPCSV typically stunts sweetpotato plants and causes either a reddening or chlorotic yellowing of middle and lower leaves. However, symptoms may also be very mild or even absent, depending perhaps, on the isolate and the conditions. In South America, SPCSV has been reported to induce mosaic symptoms in leaves. SPCSV is most commonly found in combination with SPFMV causing SPVD.

SPCSV is a phloem-associated virus transmitted by the whitefly Bemisia tabaci in the semi-persistent manner and needs feeds of several hours to be acquired or transmitted efficiently. It may also be perpetuated through cropping cycles via infected cuttings. SPCSV is generally identified in combination with SPFMV, causing the severe disease SPVD. However, SPCSV seems to gain little or nothing from this relationship as its strength and distribution in sweetpotato plants seems unaffected, though the strength of SPFMV may be some hundredfold greater in dually-infected plants.

Host range

SPCSV has only been reported on sweetpotato.  However, wild hosts have been reported to be important in Israel. In addition, SPCSV has been transmitted to a range of Ipomoea spp. including I. setosa, I. acuminata, I. hederacea, I. hederifolia, I. nil cv Scarlet O’Hara, I. purpurea, I. trichocarpa, I. trifida, I. wrightii, I. mexicana, I. Bona nox and I. hildebrandtii. It has also been transmitted to Nicotiana clevelandii, N. benthamiana and Amaranthus palmeri  and been identified in lisianthus (Eustoma grandiflorum).

Both monoclonal and polyclonal antisera have been developed against SPCSV allowing sensitive ELISA-based assays to be developed. The coat protein gene has been sequenced and both PCR and cDNA probes have also been used to detect SPCSV.

No immunity has been identified in sweetpotato though genotypes with useful levels of resistance to infection in the field have been selected by farmers and plant breeders. Sweetpotato varieties also vary in their tolerance to SPVD but it is not clear whether mild symptoms of infection are likely to be beneficial overall in a vegetatively propagated crop.

Sanitation and selection of planting material from unaffected parents help achieve control.

Ames, T., Smit, N.E.J.M., Braun, A.R., O’Sullivan, J.N., and Skoglund, L.G. 1996. Sweetpotato: Major pests diseases, and nutritional disorders. International Potato Center (CIP). Lima, Perú. 152 p.

Cohen, J., Franck, A., Vetten, H. J., Lesemann, D. E. and Loebenstein, G. 1992. Purification and properties of closterovirus-like particles associated with a whitefly-transmitted disease of sweet potato. Annals of Applied Biology. 121: 257-268.

Gibson, R. W., Mpembe, I., Alicai, T., Carey, E. E., Mwanga, R. O. M., Seal, S. E. and Vetten, H. J. 1998. Symptoms, aetiology and serological analysis of sweet potato virus disease in Uganda. Plant Pathology. 47: 95-102.

Schaefers, G. A. and Terry, E. R. 1976. Insect transmission of sweet potato disease agents in Nigeria. Phytopathology 66:642-645.

Schaefers, G. A. and Terry, E. R. 1976. Insect transmission of sweetpotato disease agents in Nigeria. Phytopathology 66:642-645.

Contributed by:  Nicole Smit and Richard Gibson

Taxonomy

Economic importance

Geographical distribution

Symptoms

Biology and ecology

Host range

Detection and inspection

Management

References