Evidence map›Paper›PMID 29686409›Full record

ArticleNature communications2018

Vibrio vulnificus quorum-sensing molecule cyclo(Phe-Pro) inhibits RIG-I-mediated antiviral innate immunity.

Wooseong Lee, Seung-Hoon Lee, Minwoo Kim, Jae-Su Moon, Geon-Woo Kim, Hae-Gwang Jung, In Hwang Kim, Ji Eun Oh, Hi Eun Jung, Heung Kyu Lee and 5 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

23 citing papers in PubMed, 47 citations in OpenAlex.

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  18. Frontiers in immunology · 2020
    Article
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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

15 authors at 4 institutions in 1 country.

Wooseong LeeDepartment of Biotechnology, Yonsei University, Seoul, 03722, Korea.
Seung-Hoon LeeDepartment of Biotechnology, Yonsei University, Seoul, 03722, Korea.
Minwoo KimDepartment of Biotechnology, Yonsei University, Seoul, 03722, Korea.
Jae-Su MoonDepartment of Biotechnology, Yonsei University, Seoul, 03722, Korea.
Geon-Woo KimDepartment of Biotechnology, Yonsei University, Seoul, 03722, Korea.
Hae-Gwang JungDepartment of Biotechnology, Yonsei University, Seoul, 03722, Korea.
In Hwang KimDepartment of Life Science, Sogang University, Seoul, 04107, Korea.
Ji Eun OhGraduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, 34141, Korea.
Hi Eun JungBiomedical Science and Engineering Interdisciplinary Program, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, 34141, Korea.
Heung Kyu LeeGraduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, 34141, Korea.ORCID http://orcid.org/0000-0002-3977-1510
Keun Bon KuCenter for Convergent Research of Emerging Virus Infection, Korea Research Institute of Chemical Technology, Daejeon, 34114, Korea.
Dae-Gyun AhnCenter for Convergent Research of Emerging Virus Infection, Korea Research Institute of Chemical Technology, Daejeon, 34114, Korea.
Seong-Jun KimCenter for Convergent Research of Emerging Virus Infection, Korea Research Institute of Chemical Technology, Daejeon, 34114, Korea.
Kun-Soo KimDepartment of Life Science, Sogang University, Seoul, 04107, Korea.
Jong-Won OhDepartment of Biotechnology, Yonsei University, Seoul, 03722, Korea. jwoh@yonsei.ac.kr.
Korea Advanced Institute of Science and Technology · KRYonsei University · KRKorea Research Institute of Chemical Technology · KRSogang University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The recognition of pathogen-derived ligands by pattern recognition receptors activates the innate immune response, but the potential interaction of quorum-sensing (QS) signaling molecules with host anti-viral defenses remains largely unknown. Here we show that the Vibrio vulnificus QS molecule cyclo(Phe-Pro) (cFP) inhibits interferon (IFN)-β production by interfering with retinoic-acid-inducible gene-I (RIG-I) activation. Binding of cFP to the RIG-I 2CARD domain induces a conformational change in RIG-I, preventing the TRIM25-mediated ubiquitination to abrogate IFN production. cFP enhances susceptibility to hepatitis C virus (HCV), as well as Sendai and influenza viruses, each known to be sensed by RIG-I but did not affect the melanoma-differentiation-associated gene 5 (MDA5)-recognition of norovirus. Our results reveal an inter-kingdom network between bacteria, viruses and host that dysregulates host innate responses via a microbial quorum-sensing molecule modulating the response to viral infection.

Indexed as

AnimalsCell Line, TumorDEAD Box Protein 58DipeptidesDisease Models, AnimalHEK293 CellsHepatocytesHost-Pathogen InteractionsHumansImmunity, InnateInterferon-betaMaleMiceMice, Inbred BALB CMice, Inbred C57BLMice, Inbred NODcyclo(phenylalanyl-prolyl)DEAD Box Protein 58DipeptidesInterferon-betaPeptides, CyclicReceptors, ImmunologicRIGI protein, human

Identifiers

PMID29686409
PMCPMC5913291
OpenAlexW2802535166

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.