Evidence map›Paper›PMID 38449860›Full record

ArticleFrontiers in immunology2024

ASFV pA151R negatively regulates type I IFN production via degrading E3 ligase TRAF6.

You Li, Li Huang, Hui Li, Yingqi Zhu, Zilong Yu, Xiaojie Zheng, Changjiang Weng, Wen-Hai Feng

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
9.6field-weighted citation impact, top 2% of its field
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

16 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. When ASFV Infection Meets the cGAS-STING Signaling Pathway.Transboundary and emerging diseases · 2024
    Review
  16. Article
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

8 authors at 3 institutions in 1 country.

You LiState Key Laboratory of Animal Biotech Breeding, China Agricultural University, Beijing, China.
Li HuangState Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute of Chinese Academy of Agricultural Sciences, Harbin, China.
Hui LiState Key Laboratory of Animal Biotech Breeding, China Agricultural University, Beijing, China.
Yingqi ZhuState Key Laboratory of Animal Biotech Breeding, China Agricultural University, Beijing, China.
Zilong YuState Key Laboratory of Animal Biotech Breeding, China Agricultural University, Beijing, China.
Xiaojie ZhengState Key Laboratory of Animal Biotech Breeding, China Agricultural University, Beijing, China.
Changjiang WengState Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute of Chinese Academy of Agricultural Sciences, Harbin, China.
Wen-Hai FengState Key Laboratory of Animal Biotech Breeding, China Agricultural University, Beijing, China.
China Agricultural University · CNChinese Academy of Agricultural Sciences · CNHarbin Veterinary Research Institute · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

African swine fever (ASF) caused by African swine fever virus (ASFV) is a highly mortal and hemorrhagic infectious disease in pigs. Previous studies have indicated that ASFV modulates interferon (IFN) production. In this study, we demonstrated that ASFV pA151R negatively regulated type I IFN production. Ectopic expression of pA151R dramatically inhibited K63-linked polyubiquitination and Ser172 phosphorylation of TANK-binding kinase 1 (TBK1). Mechanically, we demonstrated that E3 ligase TNF receptor-associated factor 6 (TRAF6) participated in the ubiquitination of TBK1 in cGAS-STING signaling pathway. We showed that pA151R interacted with TRAF6 and degraded it through apoptosis pathway, leading to the disruption of TBK1 and TRAF6 interaction. Moreover, we clarified that the amino acids H102, C109, C132, and C135 in pA151R were crucial for pA151R to inhibit type I interferon production. In addition, we verified that overexpression of pA151R facilitated DNA virus Herpes simplex virus 1 (HSV-1) replication by inhibiting IFN-β production. Importantly, knockdown of pA151R inhibited ASFV replication and enhanced IFN-β production in porcine alveolar macrophages (PAMs). Our findings will help understand how ASFV escapes host antiviral immune responses and develop effective ASFV vaccines.

Indexed as

African Swine FeverAfrican Swine Fever VirusAnimalsSwineTNF Receptor-Associated Factor 6UbiquitinationUbiquitin-Protein LigasesTNF Receptor-Associated Factor 6Ubiquitin-Protein LigasesASFVpA151RTBK1TRAF6type I IFN

Identifiers

PMID38449860
PMCPMC10914938
OpenAlexW4392001708

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.