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<p>White spot syndrome virus (WSSV) is a highly virulent pathogen that causes massive economic losses in shrimp aquaculture. Although shrimp possess an RNA interference (RNAi) antiviral defense mechanism, WSSV evades silencing, suggesting the presence of viral suppressors of RNAi (VSRs). In this study, the hypothetical protein GP172 (YP_009220646.1) was identified as a potential VSR through in silico prediction. Using a GFP-shRNA silencing reversal assay in mammalian cells, GP172 was shown to restore GFP expression, indicating its RNAi suppression function. Furthermore, docking and yeast two-hybrid (Y2H) analyses revealed interactions between GP172 and the key RNAi pathway component Argonaute 2 (AGO2). Computational analyses predicted the existence of a promoter upstream of the <i>gp172</i> gene, which harbors putative binding sites for several viral proteins, including WSV078, WSV083, WSV303, and notably, its own product WSV500 (GP172). These results suggest that <i>gp172</i> expression is likely regulated by the immediate-early proteins WSV078 and WSV083, which are predicted to form a transcriptional complex by bridging the TATA-binding protein WSV303 and the enhancer-associated factor WSV500. Collectively, these findings provide initial evidence for a WSSV-encoded VSR and its regulatory mechanism, highlighting the self-regulatory potential of GP172 and suggesting that the WSV078–VSR–AGO2 axis may represent a promising target for novel antiviral strategies in shrimp aquaculture.</p>

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Characterization of a putative RNAi suppressor encoded by white spot syndrome virus

  • 期刊论文

  • 发表日期：

    2025年11月12日

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  • Xiaotong Ren,
  • Mengting Wang,
  • Yongzhong Lu

摘要

White spot syndrome virus (WSSV) is a highly virulent pathogen that causes massive economic losses in shrimp aquaculture. Although shrimp possess an RNA interference (RNAi) antiviral defense mechanism, WSSV evades silencing, suggesting the presence of viral suppressors of RNAi (VSRs). In this study, the hypothetical protein GP172 (YP_009220646.1) was identified as a potential VSR through in silico prediction. Using a GFP-shRNA silencing reversal assay in mammalian cells, GP172 was shown to restore GFP expression, indicating its RNAi suppression function. Furthermore, docking and yeast two-hybrid (Y2H) analyses revealed interactions between GP172 and the key RNAi pathway component Argonaute 2 (AGO2). Computational analyses predicted the existence of a promoter upstream of the gp172 gene, which harbors putative binding sites for several viral proteins, including WSV078, WSV083, WSV303, and notably, its own product WSV500 (GP172). These results suggest that gp172 expression is likely regulated by the immediate-early proteins WSV078 and WSV083, which are predicted to form a transcriptional complex by bridging the TATA-binding protein WSV303 and the enhancer-associated factor WSV500. Collectively, these findings provide initial evidence for a WSSV-encoded VSR and its regulatory mechanism, highlighting the self-regulatory potential of GP172 and suggesting that the WSV078–VSR–AGO2 axis may represent a promising target for novel antiviral strategies in shrimp aquaculture.