Diagnosis and Resistance Breeding of Peanut Bud Necrosis Virus

Authors

D. V. R. Reddy, lInternational Crops Research Institute for the Semi-Arid Tropics
Satyanarayana Tatineni, USDA-ARSFollow
S. L. Dwivedi, lInternational Crops Research Institute for the Semi-Arid Tropics
A. S. Ratna, lInternational Crops Research Institute for the Semi-Arid Tropics
A. A. M. Buiel, Wageningen Agricultural University
G. V. Ranga Rao, lInternational Crops Research Institute for the Semi-Arid Tropics
S. N. Nigam, lInternational Crops Research Institute for the Semi-Arid Tropics
R. A. Naidu, lInternational Crops Research Institute for the Semi-Arid Tropics
H. T. Hsu, USDA-ARS
J. W. Demski, Georgia Experiment Station

Document Type

Article

Date of this Version

1996

Citation

Acta Horticulturae 431, 1996 - Tospoviruses and Thrips.

Comments

U.S. government work.

Abstract

The occu!fence of peanut bud necrosis (PBN) disease in India was first reported in 1968. The high incidence ofPBN disease during the 1960s coincided with largescale imports of the peanut cultivars Asiria Mwitundae and Spanish Improved, both of which are highly susceptible to PBN. Since then, a number of reports have been published in India describing bud necrosis under at least seven different names (Reddy 1988). Crop losses due to PBN have been estimated at USD89 million per year in India during 1976-1986. The disease is also currently recognized as economically important in Nepal (Sharma 1996), in Sri Lanka, and in Thailand (Wongkaew 1995).

The causal agent of PBN was originally reported as tomato spotted wilt virus (TSWV) (Ghanekar et al. 1979). Since then, methods to purify the causal virus of PBN have been developed, which facilitated the production of good quality antisera. On the basis of serological relationships, some physicochemical properties, and thrips transmission, it was shown that the causal virus of PBN in India was a distinct tospovirus that was named peanut bud necrosis virus (PBNV, Reddy et al. 1992). These results were subsequently confirmed by Adam et al. (1993). Later, monoclonal antibodies (MAbs) have been produced against the nucleocapsid (N) protein ofPBNV (Poul et al. 1992). Antibodies from nine clones failed to react with a TSWV-Iettuce (TSWV-L) isolate and with an impatiens necrotic spot virus (INSV) by triple-antibody sandwich enzyme-linked immunosorbent assay (TAS-ELISA) (coating ofPBNV polyclonal antiserum, addition of antigen followed by addition ofMAbs and antimouse IgGs conjugated to alkaline phosphatase). Of 16 MAbs produced against TSWV-L (Hsu et al. 1990), 12 H5 Al (f), 12 H5 H5 (1), and 10 C2FP (n) reacted with TSWV-L, but none reacted with PBNV in TAS-ELISA. Because PBNV and TSWV-L MAbs did not react in western blots it was not possible to test the specificity of the MAbs to glycoproteins Gland G2 or N proteins.