Emodin induces defensive autophagy against white spot syndrome virus infection via targeting the hemocyanin-mediated endoplasmic reticulum-mitochondrial crosstalk in shrimp

RNAi or ITPR and MCU inhibition phenocopied emodin, whereas exogenous HMC or ER stress activation exacerbated infection and was mitigated by emodin or MCU blockade. These findings establish HMC-anchored ER-mitochondrial contact as a central proviral vulnerability and position emodin as a practical scaffold for next-generation antivirals in aquaculture.