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Updated: Aug 6, 2026

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
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.
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.
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