Evidence map›Paper›PMID 39543624›Full record

ArticleVeterinary research2024

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.

Shuang-Shuang Zhao, Qisheng Qian, Yao Wang, Songlin Qiao, Rui Li

Abstract read
In one paragraph

Article in Veterinary research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Autophagy and porcine circovirus infection: a mini review.Frontiers in cellular and infection microbiology · 2025
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Shuang-Shuang ZhaoKey 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.
Qisheng QianInstitute for Animal Health (Key Laboratory of Animal Immunology), Henan Academy of Agricultural Sciences, Zhengzhou, 450002, Henan, China.
Yao WangInstitute for Animal Health (Key Laboratory of Animal Immunology), Henan Academy of Agricultural Sciences, Zhengzhou, 450002, Henan, China.
Songlin QiaoInstitute for Animal Health (Key Laboratory of Animal Immunology), Henan Academy of Agricultural Sciences, Zhengzhou, 450002, Henan, China. cdj565@gmail.com.
Rui LiInstitute for Animal Health (Key Laboratory of Animal Immunology), Henan Academy of Agricultural Sciences, Zhengzhou, 450002, Henan, China. lirui860620@sina.com.ORCID http://orcid.org/0000-0001-5343-3027

Funding

Agriculture Research System of China CARS-35National Natural Science Foundation of China 32172875National Natural Science Foundation of China 32272993Special Fund for Henan Agriculture Research System HARS-22-12-S
6 · The paper itself

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.

Indexed as

AutophagyInterferon Type IPorcine respiratory and reproductive syndrome virusProtein Serine-Threonine KinasesAnimalsImmunity, InnatePorcine Reproductive and Respiratory SyndromeSwineViral Nonstructural ProteinsVirus ReplicationInterferon Type IProtein Serine-Threonine KinasesViral Nonstructural ProteinsCMAIFN-INsp2PRRSVTBK1

Identifiers

PMID39543624
PMCPMC11566183

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.