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Viruses often usurp host machineries for their amplification, but it remains unclear if hosts may subvert virus proteins to regulate viral proliferation. Here, we show that the 17K protein, an important virulence factor conserved in barley yellow dwarf viruses (BYDVs) and related poleroviruses, is phosphorylated by host GRIK1‐SnRK1 kinases, with the phosphorylated 17K (P17K) capable of enhancing the abundance of virus‐derived small interfering RNAs (vsiRNAs) and thus antiviral RNAi. Furthermore, P17K interacts with barley small RNA‐degrading nuclease 1 (HvSDN1) and impedes HvSDN1‐catalyzed vsiRNA degradation. Additionally, P17K weakens the HvSDN1‐HvAGO1 interaction, thus hindering HvSDN1 from accessing and degrading HvAGO1‐carried vsiRNAs. Importantly, transgenic expression of 17K phosphomimetics (17K5D), or genome editing of SDN1, generates stable resistance to BYDV through elevating vsiRNA abundance. These data validate a novel mechanism that enhances antiviral RNAi through host subversion of a viral virulence protein to inhibit SDN1‐catalyzed vsiRNA degradation and suggest new ways for engineering BYDV‐resistant crops. Synopsis: Viruses often subvert host proteins for their amplification, but host subversion of virus proteins to regulate viral proliferation has not been reported in plants. This work shows that a plant‐viral virulence protein is phosphorylated by host kinases, with the phosphorylated form becoming an inhibitor of AGO1‐associated vsiRNAs cleavage and thus enhancing the abundance of antiviral RNAi.The 17K protein of barley yellow dwarf virus (BYDV) is phosphorylated by host GRIK1‐SnRK1 kinases.The phosphorylated 17K (P17K) interacts with host small RNA degrading nuclease 1 (HvSDN1) and Argonaute 1 (HvAGO1), and binds BYDV vsiRNA.P17K inhibits the cleavage of HvAGO1‐associated vsiRNAs by HvSDN1, thus elevating vsiRNA abundance and resulting in enhanced antiviral RNAi.Transgenic expression of a 17K phosphomimetic (17K5D), or genome editing of SDN1, generates stable resistance to BYDV through elevating vsiRNA abundance. [ABSTRACT FROM AUTHOR]