Pyrethroid insecticides act on the voltage-gated sodium channel and mutations of the channel can confer resistance in many insect species. For example, the kdr (LI014F) mutation found in domain IIS6 and the super-kdr (M918T) mutation found in the IIS4-S5 linker of the insect Drosophila melanogaster para sodium channel reduces the sensitivity of the channel to pyrethroids. Two mutations found in different pyrethroid-resistant strains of Bemisia tabaci were incorporated individually into the para wild type sodium channel of Drosophila and expressed in Xenopus laevis oocytes to investigate their effect on pyrethroid sensitivity. Voltage clamp assays showed that the M918V mutation conferred a 16-fold and a 800-fold reduction in para sensitivity to deltamethrin and permethrin respectively. The T929V mutation, caused a 2600-fold reduction in para channel sensitivity to deltamethrin. A T929M mutation, which at the equivalent residue position in the human skeletal muscle sodium channel causes Hyperkalemic Periodic Paralysis in humans, gave similar deltarnethrin insensitivity. All three mutations reduced the sensitivity of para channel populations by reducing the number of channels in the open state, to which deltamethrin and permethrin bind preferentially, and by reducing the affinity of the pyrethroid for the channel. The rat IIA voltage-gated sodium channel, which is approximately 4500-fold less sensitive to pyrethroids than the insect para sodium channel, has an isoleucine at the equivalent super-kdr residue. Replacement of this with either methionine or cysteine, increased the sensitivity of the channel to deltamethrin >80-fold and to pennethrin by 150-fold. These mutations highlight possible locations of pyrethroid binding sites and give insights into the mechanisms by which pyrethroids modify sodium channel behaviour. Kdr and super-kdr mutations are found in the housefly and a DNA diagnostic was used to show that the genotypes present in field populations reflected the selection pressure imposed by different insecticide regimes.

The present study evaluated the effect of three host plants: chickpea, Cicer arietinum, tomato, Lycopersicon esculentum and cotton, Gossypium hirsutum, on the efficacy of Helicoverpa armigera nucleopolyhedrovirus (HearNPV). The results showed that HearNPV was inactivated within one hour when sprayed on to the leaf surface of chickpea indicating that leaf surface factors on this plant were responsible for the effect. In contrast, virus that has been sprayed onto the leaf surface of cotton and tomato was not significantly affected compared to untreated HearNPV. This study also showed that HearNPV was inactivated on the chickpea leaf surface in field experiments. One compound was shown to be induced on the chickpea leaf surface in response to spraying with 0.02% Triton X-100 which was used as a surfactant. The induced compound was isolated and identified as sissotrin, and isoflavonoid. Sissotrin was shown to reduce the efficacy of HearNPV, although not by as much as when the virus was exposed to the chickpea leaf surface. The results indicated that sissotrin was partially responsible for the inactivation of HearNPV and that other compounds which accumulated on the leaf surface after spraying with HearNPV must also have an additional effect in combination with sissotrin. This is the first study to show that isoflavonoids reduce the efficacy of baculovirus against Helicoverpa armigera (Hübner) (Lepidoptera: Noctuidae). Field trials were also conducted with different low cost additives mixed with HearNPV on chickpea crop and these increased the efficacy and persistence of HearNPV under field conditions. This study may therefore help to improve biopesticide based pest management on chickpea.