FoxO-promoted peroxiredoxin1 expression induced by Helicoverpa armigera single nucleopolyhedrovirus infection mediates host development and defensive responses

Helicoverpa armigera single nucleopolyhedrovirus (HearNPV) has a long coevolutionary history with its host, exerting profound effects on larval development, physiology and immune responses, although the mechanisms mediating these effects remain unclear. We demonstrate that HearNPV infection constrains the growth and development of larvae by inducing high levels of reactive oxygen species (ROS), which increase the expression of forkhead box O transcription factor (FoxO). FoxO upregulates the expression of peroxiredoxin 1 (Prx1) which serves to regulate larval development and immune responses following HearNPV infection. Collectively, our results provide novel insights into the role of Prx1 in larval development and immunity subsequent to HearNPV infection. Further investigation of the oxidative stress induced by HearNPV in H. armigera and its interactions with host immunity could yield novel insights useful in agricultural pest control.

Automated summary

Infection of Helicoverpa armigera single nucleopolyhedrovirus (HearNPV) can restrict the growth and development of larvae by inducing reactive oxygen species (ROS) and affecting immune responses. The transcription factor forkhead box O (FoxO) upregulates the expression of peroxiredoxin 1 (Prx1), which plays a role in regulating larval development and immunity following HearNPV infection.