Evidence map›Paper›PMID 24675692›Full record

ArticlePLoS pathogens2014

Interferon regulatory factor-1 protects from fatal neurotropic infection with vesicular stomatitis virus by specific inhibition of viral replication in neurons.

Sharmila Nair, Kristin Michaelsen-Preusse, Katja Finsterbusch, Sabine Stegemann-Koniszewski, Dunja Bruder, Martina Grashoff, Martin Korte, Mario Köster, Ulrich Kalinke, Hansjörg Hauser and 1 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 43 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

11 authors at 3 institutions in 1 country.

Sharmila NairResearch Group Innate Immunity and Infection, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Kristin Michaelsen-PreusseDepartment of Cellular Neurobiology, Technical University Braunschweig, Braunschweig, Germany.
Katja FinsterbuschResearch Group Innate Immunity and Infection, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Sabine Stegemann-KoniszewskiImmune Regulation Group, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Dunja BruderImmune Regulation Group, Helmholtz Centre for Infection Research, Braunschweig, Germany; Infection Immunology Group, Department of Medical Microbiology, Otto-von-Guericke-University Magdeburg, Magdeburg, Germany.
Martina GrashoffResearch Group Innate Immunity and Infection, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Martin KorteDepartment of Cellular Neurobiology, Technical University Braunschweig, Braunschweig, Germany; Research Group Neuroinflammation and Neurodegeneration, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Mario KösterDepartment of Gene Regulation and Differentiation, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Ulrich KalinkeInstitute for Experimental Infection Research, TWINCORE, Hannover, Germany.
Hansjörg HauserDepartment of Gene Regulation and Differentiation, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Andrea KrögerResearch Group Innate Immunity and Infection, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Helmholtz Centre for Infection Research · DECenter for Experimental and Clinical Infection Research · DETechnische Universität Braunschweig · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The innate immune system protects cells against invading viral pathogens by the auto- and paracrine action of type I interferon (IFN). In addition, the interferon regulatory factor (IRF)-1 can induce alternative intrinsic antiviral responses. Although both, type I IFN and IRF-1 mediate their antiviral action by inducing overlapping subsets of IFN stimulated genes, the functional role of this alternative antiviral action of IRF-1 in context of viral infections in vivo remains unknown. Here, we report that IRF-1 is essential to counteract the neuropathology of vesicular stomatitis virus (VSV). IFN- and IRF-1-dependent antiviral responses act sequentially to create a layered antiviral protection program against VSV infections. Upon intranasal infection, VSV is cleared in the presence or absence of IRF-1 in peripheral organs, but IRF-1-/- mice continue to propagate the virus in the brain and succumb. Although rapid IFN induction leads to a decline in VSV titers early on, viral replication is re-enforced in the brains of IRF-1-/- mice. While IFN provides short-term protection, IRF-1 is induced with delayed kinetics and controls viral replication at later stages of infection. IRF-1 has no influence on viral entry but inhibits viral replication in neurons and viral spread through the CNS, which leads to fatal inflammatory responses in the CNS. These data support a temporal, non-redundant antiviral function of type I IFN and IRF-1, the latter playing a crucial role in late time points of VSV infection in the brain.

Indexed as

AnimalsEnzyme-Linked Immunosorbent AssayFluorescent Antibody TechniqueImmunohistochemistryInterferon Regulatory Factor-1MiceMice, Inbred C57BLMice, KnockoutNeuronsReal-Time Polymerase Chain ReactionVesicular StomatitisVesiculovirusVirus ReplicationInterferon Regulatory Factor-1Irf1 protein, mouse

Identifiers

PMID24675692
PMCPMC3968136
OpenAlexW2087548206

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.