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NUDT7 Modulates the UBA52-SREBF1 Signaling Axis to Promote PRRSV Replication via Lipid Synthesis.

Yuchao Yan1, Changyan Li1, Junyang Zhang1

  • 1School of Life Sciences, Faculty of Medicine, Tianjin University, Tianjin, 300072, China.

International Journal of Biological Sciences
|January 29, 2026
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Summary

NUDT7 protein promotes Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) replication by reprogramming lipid metabolism and inhibiting immune signaling. Targeting NUDT7 offers a potential therapeutic strategy against PRRSV infection.

Keywords:
NUDT7PRRSVinnate immunitylipid metabolismubiquitin

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Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • Understanding host factors in viral infections is key for developing therapies.
  • Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) utilizes host metabolic reprogramming and immunosuppression.
  • Host factors coordinating these processes during PRRSV infection remain unclear.

Purpose of the Study:

  • To elucidate the role of NUDT7 in PRRSV replication.
  • To investigate the mechanisms by which NUDT7 influences host metabolism and immune response during PRRSV infection.

Main Methods:

  • Analysis of NUDT7 expression during PRRSV infection.
  • Investigating the interaction between NUDT7, UBA52, and SREBF1.
  • Assessing the impact of NUDT7 on lipid droplet synthesis and interferon signaling.

Main Results:

  • NUDT7 expression is upregulated by ETS1 during PRRSV infection.
  • NUDT7 enhances PRRSV replication by promoting lipid droplet synthesis and stabilizing SREBF1.
  • NUDT7 targets UBA52 for degradation, inhibiting polyubiquitination and stabilizing SREBF1.
  • NUDT7 suppresses type I interferon signaling and interferon-stimulated genes, aiding viral immune evasion.

Conclusions:

  • The NUDT7-UBA52-SREBF1 axis drives metabolic reprogramming favorable for PRRSV replication.
  • NUDT7 plays a critical role in both metabolic adaptation and immune evasion during PRRSV infection.
  • NUDT7 represents a potential therapeutic target for PRRSV, suggesting novel metabolic-immune antiviral strategies.