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Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
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Published on: March 2, 2014

Soluble triggering receptor expressed on myeloid cells 2 restrained PRRSV replication via interfering PRRSV binding

Zhenbang Zhu1, Meng Zhang1, Yuqian Xu1

  • 1Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, College of Veterinary Medicine, Yangzhou University, Yangzhou 225009, PR China; Jiangsu Interdisciplinary Center for Zoonoses and Biosafety, Yangzhou University, Yangzhou 225009, PR China; Jiangsu Key Laboratory of Zoonosis, Yangzhou University, Yangzhou 225009, PR China.

Veterinary Microbiology
|July 21, 2026
PubMed

Insights

Soluble triggering receptor expressed on myeloid cells 2 (sTREM2) inhibits porcine reproductive and respiratory syndrome virus (PRRSV) replication. This study reveals sTREM2 binds PRRSV GP2a, blocking viral entry and activating immune pathways for potential clinical applications.

Area of Science:

  • Veterinary Virology
  • Immunology
  • Molecular Biology

Background:

  • Porcine reproductive and respiratory syndrome virus (PRRSV) significantly impacts the global swine industry.
  • PRRSV infection is known to increase soluble triggering receptor expressed on myeloid cells 2 (sTREM2) levels in plasma.

Purpose of the Study:

  • To investigate the role of sTREM2 in regulating PRRSV replication.
  • To elucidate the underlying mechanisms of sTREM2's effect on PRRSV.

Main Methods:

  • Exogenous expression and purification of sTREM2.
  • In vitro assays to assess PRRSV replication in the presence of sTREM2.
  • Analysis of sTREM2 interaction with PRRSV envelope protein GP2a.
  • Investigation of NF-κB signaling pathway activation and cytokine expression.

Main Results:

  • Exogenously supplied sTREM2 demonstrated an inhibitory effect on PRRSV replication in vitro.
  • sTREM2 was found to interact with the PRRSV envelope protein GP2a, with specific amino acid sites (S112/S116/T120) being crucial for binding.
  • This interaction impeded the viral binding stage, thereby inhibiting PRRSV replication.
  • sTREM2 promoted NF-κB pathway activation, increased proinflammatory cytokines, and elevated type I interferons, contributing to PRRSV suppression.

Conclusions:

  • sTREM2 exhibits significant inhibitory effects against PRRSV replication.
  • The interaction between sTREM2 and PRRSV GP2a is a key mechanism for this inhibition.
  • sTREM2 holds potential for clinical applications in managing PRRSV infections.
Keywords:
Antiviral mechanismNF-ĸB signaling pathwayPRRSVProinflammatory cytokinesSoluble TREM2

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