Grass carp hemorrhagic disease (GCHD) induced by grass carp reovirus (GCRV) causes severe economic losses in the grass carp aquaculture industry, and breeding for GCRV resistance is of great significance for disease prevention and genetic improvement. In this study, we performed parallel GCRV-II infection experiments on wild-type and GCRV-resistant grass carp to investigate the key immune mechanisms underlying GCRV-II infection and screen for differentially expressed genes (DEGs) between the two groups after viral infection. Functional annotation revealed a set of core genes involved in host antiviral immune responses, such as TLR3, NLRP3, RIG-I, IRF3, Mex3C, IFIT1, TRIM25, and ISG15. The differential expression of these immune-related genes may indirectly reflect the disease-resistance capacity of resistant grass carp. This transcriptional pattern suggests that resistant fish may maintain a more balanced immune homeostasis rather than mounting excessive inflammatory responses during viral infection. Collectively, this study investigates potential antiviral-immune mechanisms in grass carp and offers perspectives for GCRV-resistant grass carp breeding.