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Insight into the regulation of the Nrf2 pathway in response to ascovirus infection in Spodoptera exigua.

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BACKGROUND Ascoviruses are a kind of entomopathogenic microorganisms with high biological pest control potential, which is expected to contribute in natural control of lepidopteran pests. However, knowledge of the molecular… Click to show full abstract

BACKGROUND Ascoviruses are a kind of entomopathogenic microorganisms with high biological pest control potential, which is expected to contribute in natural control of lepidopteran pests. However, knowledge of the molecular mechanism underlying the biocidal activity of ascovirus on its host insects are still limited. RESULTS In this study, the relative enzyme activity of superoxide dismutase and peroxidase as well as the expression level of Spodoptera exigua peroxidase (SePOD) in was found to be significantly increased at 6 hours post infection (hpi) with Heliothis virescens ascovirus 3h (HvAV-3h). Moreover, the H2 O2 accumulation and enhanced expression of NADPH Oxidase (SeNOX) was also observed. Additionally, nuclear factor erythroid 2-related factor 2 (SeNrf2) and muscle aponeurosis fibromatosis (SeMaf) were overexpressed when infected with HvAV-3h. silencing of SeNrf2 decreased the expression of SePOD, the mortality of SeNrf2-silenced larvae increased, and the viral genome copy number also increased. Further RNAi of SeNOX significantly decreased the expression of SeNrf2 and SePOD and therefore increased the mortality and viral genome copy number of the ascovirus infected host. CONCLUSION HvAV-3h activated Nrf2/ARE pathway of S. exigua, and ROS was found to respond to ascovirus infection by regulating the alteration of antioxidant enzyme genes mediated by the host Nrf2/ARE pathway. These findings enhance our knowledge of ascovirus-host interaction and lay the foundation for the application of ascoviruses in biological pest control.

Keywords: spodoptera exigua; ascovirus; ascovirus infection; nrf2 pathway

Journal Title: Pest management science
Year Published: 2022

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