Evidence map›Paper›PMID 34851144›Full record

ArticleJournal of virology2022

Induction of HOXA3 by Porcine Reproductive and Respiratory Syndrome Virus Inhibits Type I Interferon Response through Negative Regulation of HO-1 Transcription.

Yingtong Feng, Xuyang Guo, Hong Tian, Yuan He, Yang Li, Xuelian Jiang, Haixue Zheng, Shuqi Xiao

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

24 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Cobalt Protoporphyrin Blocks EqHV-8 Infection via IFN-α/β Production.Animals : an open access journal from MDPI · 2023
    Article
  18. Article
  19. Article
  20. 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 2 institutions in 1 country.

Yingtong Feng *College of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, China.
Xuyang Guo *College of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, China.
Hong Tian *State Key Laboratory of Veterinary Etiological Biology, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, Gansu, China.
Yuan HeCollege of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, China.
Yang LiCollege of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, China.
Xuelian JiangCollege of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, China.
Haixue ZhengState Key Laboratory of Veterinary Etiological Biology, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, Gansu, China.ORCID 0000-0001-6850-1379
Shuqi XiaoCollege of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, China.ORCID 0000-0002-6468-2608
Northwest A&F University · CNLanzhou Veterinary Research Institute · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type I interferons (IFN-Is) play a key role in host defense against virus infection, but porcine reproductive and respiratory syndrome virus (PRRSV) infection does not effectively activate IFN-I response, and the underlying molecular mechanisms are poorly characterized. In this study, a novel transcription factor of the heme oxygenase-1 (HO-1) gene, homeobox A3 (HOXA3), was screened and identified. Here, we found that HOXA3 was significantly increased during PRRSV infection. We demonstrated that HOXA3 promotes PRRSV replication by negatively regulating the HO-1 gene transcription, which is achieved by regulating IFN-I production. A detailed analysis showed that PRRSV exploits HOXA3 to suppress beta interferon (IFN-β) and IFN-stimulated gene (ISG) expression in host cells. We also provide direct evidence that the activation of IFN-I by HO-1 depends on its interaction with IRF3. Then we further proved that a deficiency of HOXA3 promoted the HO-1-IRF3 interaction and subsequently enhanced IRF3 phosphorylation and nuclear translocation in PRRSV-infected cells. These data suggest that PRRSV uses HOXA3 to negatively regulate the transcription of the HO-1 gene to suppress the IFN-I response for immune evasion.

Indexed as

Gene Expression RegulationAnimalsBinding SitesHeme Oxygenase-1Homeodomain ProteinsHost-Pathogen InteractionsInterferon Type IPorcine Reproductive and Respiratory SyndromePorcine respiratory and reproductive syndrome virusProtein BindingProtein TransportSwineTranscription FactorsVirus ReplicationHeme Oxygenase-1Homeodomain ProteinsInterferon Type ITranscription FactorsHO-1HOXA3IFN-Iimmune evasionIRF3PRRSVregulatory transcription

Identifiers

PMID34851144
PMCPMC8827019
OpenAlexW3217327019

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.