Evidence map›Paper›PMID 27254596›Full record

ArticleVirology2016

Rapid induction and persistence of paracrine-induced cellular antiviral states arrest viral infection spread in A549 cells.

Emily A Voigt, Adam Swick, John Yin

Open access · greenAbstract read
In one paragraph

Article in Virology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed, 36 citations in OpenAlex.

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  6. The kinetics of SARS-CoV-2 infection based on a human challenge study.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  20. Quantitative profiling of innate immune activation by viral infection in single cells.Integrative biology : quantitative biosciences from nano to macro · 2017
    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

3 authors at 1 institution in 1 country.

Emily A VoigtSystems Biology Theme, Wisconsin Institute for Discovery, University of Wisconsin-Madison, Madison, WI, USA; Department of Chemical and Biological Engineering, University of Wisconsin-Madison, Madison, WI, USA.
Adam SwickSystems Biology Theme, Wisconsin Institute for Discovery, University of Wisconsin-Madison, Madison, WI, USA; Department of Chemical and Biological Engineering, University of Wisconsin-Madison, Madison, WI, USA.
John YinSystems Biology Theme, Wisconsin Institute for Discovery, University of Wisconsin-Madison, Madison, WI, USA; Department of Chemical and Biological Engineering, University of Wisconsin-Madison, Madison, WI, USA. Electronic address: john.yin@wisc.edu.
Wisconsin Institutes for Discovery · US

Funding

Wisconsin Infant Study Cohort (WISC)U19AI104317 · NIAID · UNIVERSITY OF WISCONSIN-MADISON · PI James E. Gern · 2013 to 2026
$22.5M
Virology Training ProgramT32AI078985 · NIAID · UNIVERSITY OF WISCONSIN-MADISON · PI LAMBERT, PAUL F. · 2009 to 2018
$3.3M
Evolution of Virus-Host InteractionsR01AI091646 · NIAID · UNIVERSITY OF WISCONSIN-MADISON · PI YIN, JOHN · 2011 to 2015
$2.0M
NIAID NIH HHS R01 AI091646NIAID NIH HHS T32 AI078985NIAID NIH HHS U19 AI104317
6 · The paper itself

Abstract

The virus/host interaction is a complex interplay between pro- and anti-viral factors that ultimately determines the spread or halt of virus infections in tissues. This interplay develops over multiple rounds of infection. The purpose of this study was to determine how cellular-level processes combine to impact the spatial spread of infection. We measured the kinetics of virus replication (VSV), antiviral paracrine signal upregulation and secretion, spatial spread of virus and paracrine antiviral signaling, and inhibition of virus production in antiviral-exposed A549 human lung epithelial cells. We found that initially infected cells released antiviral signals 4-to-7h following production of virus. However, the subsequent rapid dissemination of signal and fast induction of a robust and persistent antiviral state ultimately led to a suppression of infection spread. This work shows how cellular responses to infection and activation of antiviral responses can integrate to ultimately control infection spread across host cell populations.

Indexed as

Cell Cycle CheckpointsHost-Pathogen InteractionsParacrine CommunicationVirus Physiological PhenomenaVirus ReplicationA549 CellsAntiviral AgentsCells, CulturedCytokinesHumansImmunity, InnateAntiviral AgentsCytokinesA549 cellsAntiviral stateInfection spreadInterferonParacrine signalingVirus spread

Identifiers

PMID27254596
PMCPMC5159750
OpenAlexW2417702235

What OpenQuestion holds

Textmetadata
LicenceTDM
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.