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

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 strateg...

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Main Authors: Shuang-shuang Zhao, Qisheng Qian, Yao Wang, Songlin Qiao, Rui Li
Format: Article
Language:English
Published: BMC 2024-11-01
Series:Veterinary Research
Subjects:
Online Access:https://doi.org/10.1186/s13567-024-01392-w
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author Shuang-shuang Zhao
Qisheng Qian
Yao Wang
Songlin Qiao
Rui Li
author_facet Shuang-shuang Zhao
Qisheng Qian
Yao Wang
Songlin Qiao
Rui Li
author_sort Shuang-shuang Zhao
collection DOAJ
description 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.
format Article
id doaj-art-c697a7962f2d4831be10d9b1c7d54f55
institution Kabale University
issn 1297-9716
language English
publishDate 2024-11-01
publisher BMC
record_format Article
series Veterinary Research
spelling doaj-art-c697a7962f2d4831be10d9b1c7d54f552024-11-17T12:42:24ZengBMCVeterinary Research1297-97162024-11-0155111510.1186/s13567-024-01392-wPorcine reproductive and respiratory syndrome virus degrades TANK-binding kinase 1 via chaperon-mediated autophagy to suppress type I interferon production and facilitate viral proliferationShuang-shuang Zhao0Qisheng Qian1Yao Wang2Songlin Qiao3Rui Li4Key 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 UniversityInstitute for Animal Health (Key Laboratory of Animal Immunology), Henan Academy of Agricultural SciencesInstitute for Animal Health (Key Laboratory of Animal Immunology), Henan Academy of Agricultural SciencesInstitute for Animal Health (Key Laboratory of Animal Immunology), Henan Academy of Agricultural SciencesInstitute for Animal Health (Key Laboratory of Animal Immunology), Henan Academy of Agricultural SciencesAbstract 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.https://doi.org/10.1186/s13567-024-01392-wPRRSVNsp2TBK1IFN-ICMA
spellingShingle Shuang-shuang Zhao
Qisheng Qian
Yao Wang
Songlin Qiao
Rui Li
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
Veterinary Research
PRRSV
Nsp2
TBK1
IFN-I
CMA
title 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
title_full 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
title_fullStr 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
title_full_unstemmed 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
title_short 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
title_sort 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
topic PRRSV
Nsp2
TBK1
IFN-I
CMA
url https://doi.org/10.1186/s13567-024-01392-w
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