Diagnosis and Resistance Breeding of Peanut Bud Necrosis Virus

he occurrence of peanut bud necrosis (PBN) disease in India was first reported in 1968. The high incidence of PBN disease during the 1960s coincided with large-scale 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 of PBNV (Poul et al. 1992). Antibodies from nine clones failed to react with a TSWV-lettuce (TSWV-L) isolate and with an impatiens necrotic spot virus (INSV) by triple-antibody sandwich enzyme-linked immunosorbent assay (TAS-ELISA) (coating of PBNV polyclonal antiserum, addition of antigen followed by addition of MAbs 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