SePGRP-SA promotes antiviral immunity in Spodoptera exigua via Toll pathway activation

Peptidoglycan recognition proteins (PGRPs) are essential components of innate immunity that are highly conserved in both insects and mammals. While their roles in antibacterial and antifungal defense have been extensively investigated, their contributions to antiviral immunity remain largely uncharacterized. Here, we show that SePGRP-SA is predominantly expressed in the fat body of Spodoptera exigua and is significantly upregulated following infection with Spodoptera exigua multiple nucleopolyhedrovirus (SeMNPV). Overexpression of SePGRP-SA in S. exigua cells activates the Toll signaling pathway, induces the expression of antimicrobial peptides (AMPs), including Attacin2, Attacin3, Gloverin, Moricin, Defensin1, and Lebocin, and enhances antiviral defense against SeMNPV infection. Conversely, RNAi-mediated knockdown of SePGRP-SA in S. exigua cells suppressed Toll pathway activation, reduced AMP expression, and impaired antiviral responses against SeMNPV. Moreover, in vivo silencing of SePGRP-SA significantly increased the susceptibility and mortality of S. exigua larvae following SeMNPV infection. Notably, SePGRP-SA overexpression did not activate the immune deficiency (IMD) pathway. Collectively, these findings identify SePGRP-SA as a key mediator of antiviral immunity in S. exigua through Toll pathway activation and AMP induction.