Evidence map›Paper›PMID 33730651›Full record

ArticleVirology2021

Influenza A virus NS1 induces degradation of sphingosine 1-phosphate lyase to obstruct the host innate immune response.

Jennifer J Wolf, Chuan Xia, Caleb J Studstill, Hanh Ngo, Steven L Brody, Paul E Anderson, Bumsuk Hahm

Open access · greenAbstract read
In one paragraph

Article in Virology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

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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

7 authors at 4 institutions in 2 countries.

Jennifer J WolfDepartment of Surgery, University of Missouri, Columbia, MO, 65212, USA; Department of Molecular Microbiology and Immunology, University of Missouri, Columbia, MO, 65212, USA.
Chuan XiaDepartment of Surgery, University of Missouri, Columbia, MO, 65212, USA; Department of Molecular Microbiology and Immunology, University of Missouri, Columbia, MO, 65212, USA; Present Address: State Key Laboratory of Microbial Technology, Shandong University, Qingdao, 266237, China.
Caleb J StudstillDepartment of Surgery, University of Missouri, Columbia, MO, 65212, USA; Department of Molecular Microbiology and Immunology, University of Missouri, Columbia, MO, 65212, USA.
Hanh NgoDepartment of Surgery, University of Missouri, Columbia, MO, 65212, USA; Department of Molecular Microbiology and Immunology, University of Missouri, Columbia, MO, 65212, USA.
Steven L BrodyDepartment of Medicine, Washington University School of Medicine, St. Louis, MO, 63110, USA.
Paul E AndersonLaboratory for Infectious Disease Research, University of Missouri, Columbia, MO, 65212, USA.
Bumsuk HahmDepartment of Surgery, University of Missouri, Columbia, MO, 65212, USA; Department of Molecular Microbiology and Immunology, University of Missouri, Columbia, MO, 65212, USA. Electronic address: hahmb@health.missouri.edu.
University of Missouri · USShandong University · CNUniversity of Missouri Health System · USWashington University in St. Louis · US

Funding

Control of influenza virus by sphingolipid metabolismR01AI091797 · NIAID · UNIVERSITY OF MISSOURI-COLUMBIA · PI HAHM, BUMSUK · 2011 to 2015
$1.8M
NIAID NIH HHS R01 AI091797
6 · The paper itself

Abstract

The type I interferon (IFN)-mediated innate immune response is one of the central obstacles influenza A virus (IAV) must overcome in order to successfully replicate within the host. We have previously shown that sphingosine 1-phosphate (S1P) lyase (SPL) enhances IKKϵ-mediated type I IFN responses. Here, we demonstrate that the nonstructural protein 1 (NS1) of IAV counteracts the SPL-mediated antiviral response by inducing degradation of SPL. SPL was ubiquitinated and downregulated upon IAV infection or NS1 expression, whereas NS1-deficient IAV failed to elicit SPL ubiquitination or downregulation. Transiently overexpressed SPL increased phosphorylation of IKKϵ, resulting in enhanced expression of type I IFNs. However, this induction was markedly inhibited by IAV NS1. Collectively, this study reveals a novel strategy employed by IAV to subvert the type I IFN response, providing new insights into the interplay between IAV and host innate immunity.

Indexed as

Immunity, InnateProteolysisA549 CellsAldehyde-LyasesDown-RegulationHEK293 CellsHost Microbial InteractionsHumansImmune EvasionInfluenza A virusInfluenza, HumanPhosphorylationUbiquitinationViral Nonstructural ProteinsAldehyde-LyasesINS1 protein, influenza virussphingosine 1-phosphate lyase (aldolase)Viral Nonstructural ProteinsInfluenza virusNonstructural protein 1Protein degradationSphingosine-1-phosphate lyaseType I interferonUbiquitinationViral immune evasion

Identifiers

PMID33730651
PMCPMC8109848
OpenAlexW3139302837

What OpenQuestion holds

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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.