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<p>Vesicular stomatitis virus (VSV) is a zoonotic infectious disease that severely impacts the livestock economy. Infection causes vesicle formation, epithelial cell lysis, and severe interstitial edema, accompanied by inflammatory cell infiltration. It can also infect humans&#xa0;and result in a&#xa0;3 to 5-day illness&#xa0;characterized by fever, headache, fatigue, and muscle aches. (Phosphoribosyl pyrophosphate synthetase 2) PRPS2, a core rate-limiting enzyme in purine and pyrimidine nucleotide biosynthesis, is a key regulator of nucleotide metabolism. In this study, we found that knockdown of PRPS2 significantly attenuated VSV-GFP infection efficiency and suppressed viral replication. Conversely, overexpression of PRPS2 promoted VSV-GFP replication. Further mechanistic exploration revealed that PRPS2 knockdown enhanced IRF3 phosphorylation and upregulated the transcription of IFN-β, CXCL10, and ISG56. This study demonstrates that PRPS2 likely regulates the host innate immune response by modulating IRF3 phosphorylation, thereby influencing VSV replication. These findings reveal the role of PRPS2 in host antiviral immunity and deepen the theoretical understanding of VSV–host interactions.</p>

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A preliminary study on the regulatory role of phosphoribosyl pyrophosphate synthetase 2 in vesicular stomatitis virus infection

  • 期刊论文

  • 发表日期：

    2025年12月11日

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  • Nuo Xu,
  • Shuaichen Li,
  • Xiangbo Meng,
  • Hongkun Li,
  • Sunxin Zhou,
  • Hengxin Wang,
  • Anping Li,
  • Xinjing Wang,
  • Tong Zhang

摘要

Vesicular stomatitis virus (VSV) is a zoonotic infectious disease that severely impacts the livestock economy. Infection causes vesicle formation, epithelial cell lysis, and severe interstitial edema, accompanied by inflammatory cell infiltration. It can also infect humans and result in a 3 to 5-day illness characterized by fever, headache, fatigue, and muscle aches. (Phosphoribosyl pyrophosphate synthetase 2) PRPS2, a core rate-limiting enzyme in purine and pyrimidine nucleotide biosynthesis, is a key regulator of nucleotide metabolism. In this study, we found that knockdown of PRPS2 significantly attenuated VSV-GFP infection efficiency and suppressed viral replication. Conversely, overexpression of PRPS2 promoted VSV-GFP replication. Further mechanistic exploration revealed that PRPS2 knockdown enhanced IRF3 phosphorylation and upregulated the transcription of IFN-β, CXCL10, and ISG56. This study demonstrates that PRPS2 likely regulates the host innate immune response by modulating IRF3 phosphorylation, thereby influencing VSV replication. These findings reveal the role of PRPS2 in host antiviral immunity and deepen the theoretical understanding of VSV–host interactions.