Evidence map›Paper›PMID 33361422›Full record

ArticleJournal of virology2021

DDIT3 Targets Innate Immunity via the DDIT3-OTUD1-MAVS Pathway To Promote Bovine Viral Diarrhea Virus Replication.

Song Wang, Peili Hou, Wei Pan, Wenqi He, Daniel Chang He, Hongmei Wang, Hongbin He

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
10.2field-weighted citation impact, top 1% 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

37 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Research progress of DUB enzyme in breast cancer.Clinical and experimental medicine · 2025
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. PBLD enhances antiviral innate immunity by promoting the p53-USP4-MAVS signaling axis.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

7 authors at 2 institutions in 1 country.

Song WangRuminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, China.
Peili HouRuminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, China.
Wei PanRuminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, China.
Wenqi HeKey Laboratory of Zoonosis Research, Ministry of Education, College of Veterinary Medicine, Jilin University, Changchun, China.
Daniel Chang HeInternational Department, High School Attached to Shandong Normal University, Jinan, China.
Hongmei WangRuminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, China hongmeiwang@sdnu.edu.cn hongbinhe@sdnu.edu.cn.
Hongbin HeRuminant Diseases Research Center, College of Life Sciences, Shandong Normal University, Jinan, China hongmeiwang@sdnu.edu.cn hongbinhe@sdnu.edu.cn.ORCID 0000-0002-7438-0638
Shandong Normal University · CNJilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA damage-inducible transcript 3 (DDIT3) plays important roles in endoplasmic reticulum (ER) stress-induced apoptosis and autophagy, but its role in innate immunity is not clear. Here, we report that DDIT3 inhibits the antiviral immune response during bovine viral diarrhea virus (BVDV) infection by targeting mitochondrial antiviral signaling (MAVS) in Madin-Darby bovine kidney (MDBK) cells and in mice. BVDV infection induced high DDIT3 mRNA and protein expression. DDIT3 overexpression inhibited type I interferon (IFN-I) and IFN-stimulated gene production, thereby promoting BVDV replication, while DDIT3 knockdown promoted the antiviral innate immune response to suppress viral replication. DDIT3 promoted NF-κB-dependent ovarian tumor (OTU) deubiquitinase 1 (OTUD1) expression. Furthermore, OTUD1 induced upregulation of the E3 ubiquitin ligase Smurf1 by deubiquitinating Smurf1, and Smurf1 degraded MAVS in MDBK cells in a ubiquitination-dependent manner, ultimately inhibiting IFN-I production. Moreover, knocking out DDIT3 promoted the antiviral innate immune response to reduce BVDV replication and pathological changes in mice. These findings provide direct insights into the molecular mechanisms by which DDIT3 inhibits IFN-I production by regulating MAVS degradation.

Indexed as

Immunity, InnateVirus ReplicationAdaptor Proteins, Signal TransducingAnimalsAntiviral AgentsCattleDiarrhea Virus 1, Bovine ViralGene Expression RegulationHost-Pathogen InteractionsInterferon Type IMiceNF-kappa BSignal TransductionTranscription Factor CHOPUbiquitinationUbiquitin-Protein LigasesAdaptor Proteins, Signal TransducingAntiviral AgentsInterferon Type INF-kappa BTranscription Factor CHOPUbiquitin-Protein LigasesUbiquitin-Specific ProteasesBVDVDDIT3degradationinnate immunityMAVSOTUD1

Identifiers

PMID33361422
PMCPMC8094964
OpenAlexW3117831989

What OpenQuestion holds

Textmetadata
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.