2. Academic Validation
  3. Porcine reproductive and respiratory syndrome virus degrades TANK-binding kinase 1 via chaperon-mediated autophagy to suppress type I interferon production and facilitate viral proliferation

Porcine reproductive and respiratory syndrome virus degrades TANK-binding kinase 1 via chaperon-mediated autophagy to suppress type I interferon production and facilitate viral proliferation

  • Vet Res. 2024 Nov 14;55(1):151. doi: 10.1186/s13567-024-01392-w.
Shuang-Shuang Zhao 1 2,  Qisheng Qian 2,  Yao Wang 2,  Songlin Qiao 3,  Rui Li 4
Affiliations

Affiliations

  • 1 Key Laboratory of Applied Technology On Green-Eco-Healthy Animal Husbandry of Zhejiang Province, Zhejiang Provincial Engineering Laboratory for Animal Health Inspection & Internet Technology, Zhejiang International Science and Technology Cooperation Base for Veterinary Medicine and Health Management, China-Australia Joint Laboratory for Animal Health Big Data Analytics, College of Animal Science and Technology & College of Veterinary Medicine of Zhejiang A&F University, Hangzhou, 311300, Zhejiang, China.
  • 2 Institute for Animal Health (Key Laboratory of Animal Immunology), Henan Academy of Agricultural Sciences, Zhengzhou, 450002, Henan, China.
  • 3 Institute for Animal Health (Key Laboratory of Animal Immunology), Henan Academy of Agricultural Sciences, Zhengzhou, 450002, Henan, China. cdj565@gmail.com.
  • 4 Institute for Animal Health (Key Laboratory of Animal Immunology), Henan Academy of Agricultural Sciences, Zhengzhou, 450002, Henan, China. lirui860620@sina.com.
PMID: 39543624 DOI: 10.1186/s13567-024-01392-w
Abstract

Porcine reproductive and respiratory syndrome virus (PRRSV) has led to significant economic losses in the global swine industry. Type I interferon (IFN-I) plays a crucial role in the host's resistance to PRRSV Infection. Despite extensive research showing that PRRSV employs multiple strategies to antagonise IFN-I induction, the underlying mechanisms remain to be fully elucidated. In this study, we have discovered that PRRSV inhibits the production of IFN-I by degrading TANK-binding kinase 1 (TBK1) through chaperon-mediated Autophagy (CMA). From a mechanistic standpoint, PRRSV nonstructural protein 2 (Nsp2) increases the interaction between the heat shock protein member 8 (HSPA8) and TBK1. This interaction leads to the translocation of TBK1 into lysosomes for degradation, mediated by lysosomal-associated membrane protein 2A (LAMP2A). As a result, the downstream activation of IFN regulatory factor 3 (IRF3) and the production of IFN-I are hindered. Together, these results reveal a new mechanism by which PRRSV suppresses host innate immunity and contribute to the development of new Antiviral strategies against the virus.

Keywords

CMA; IFN-I; Nsp2; PRRSV; TBK1.

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