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Viruses have evolved sophisticated strategies to evade host immune defenses, often targeting conserved signaling pathways. In shrimp, the NF-κB signaling pathway is crucial for antiviral immunity, yet its regulation during White Spot Syndrome Virus (WSSV) infection remains poorly understood. Here, we identify and characterize wsv100, an immediate-early (IE) protein of WSSV, as a key antagonist of the NF-κB pathway. wsv100 interacts directly with the transcription factor Dorsal, preventing Dorsal phosphorylation by Pelle kinase. This inhibition suppresses Dorsal’s nuclear translocation and downstream expression of antimicrobial peptides (AMPs), essential for antiviral defense. Knockdown of wsv100 reduced WSSV replication, increased Dorsal phosphorylation, and enhanced AMP expression, leading to higher survival rates in infected shrimp. Conversely, wsv100 overexpression promoted WSSV replication and AMPs suppression. These findings reveal a novel immune evasion mechanism by which WSSV subverts the NF-κB pathway and highlight the evolutionary arms race between hosts and viruses. This study enhances our understanding of host-virus interactions and offers potential targets for antiviral strategies in shrimp aquaculture.病毒已演化出复杂的免疫逃逸策略，且常靶向保守的信号通路。在虾类中，核因子κB（NF-κB）信号通路是抗病毒免疫的关键通路，然而白斑综合征病毒（White Spot Syndrome Virus, WSSV）感染过程中该通路的调控机制仍不甚明确。本研究鉴定并表征了WSSV的即刻早期（immediate-early, IE）蛋白wsv100，证实其为NF-κB通路的关键拮抗剂。wsv100可与转录因子Dorsal直接结合，阻断佩勒激酶（Pelle kinase）对Dorsal的磷酸化修饰。该抑制作用可阻碍Dorsal的核转位，并下调下游抗菌肽（antimicrobial peptides, AMPs）的表达，而抗菌肽是宿主抗病毒防御的核心效应分子。敲低wsv100可抑制WSSV的复制，提升Dorsal的磷酸化水平，并增强抗菌肽的表达，最终使感染病毒的虾类存活率显著升高。反之，过表达wsv100则会促进WSSV的复制并抑制抗菌肽的表达。上述研究结果揭示了WSSV通过劫持NF-κB通路实现免疫逃逸的全新机制，凸显了宿主与病毒之间的演化军备竞赛。本研究加深了学界对宿主-病毒互作关系的理解，同时为虾类水产养殖中的抗病毒防控策略提供了潜在靶点。