Evidence map›Paper›PMID 34262037›Full record

ArticleNature communications2021

Intracellular lipid droplet accumulation occurs early following viral infection and is required for an efficient interferon response.

E A Monson, K M Crosse, M Duan, W Chen, R D O'Shea, L M Wakim, J M Carr, D R Whelan, K J Helbig

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
13.0field-weighted citation impact, top 1% 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

87 citing papers in PubMed, 133 citations in OpenAlex.

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27 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

E A MonsonDepartment of Physiology, Anatomy and Microbiology, School of Life Sciences, La Trobe University, Melbourne, VIC, Australia.ORCID http://orcid.org/0000-0001-5632-9575
K M CrosseDepartment of Physiology, Anatomy and Microbiology, School of Life Sciences, La Trobe University, Melbourne, VIC, Australia.
M DuanLa Trobe Institute for Molecular Science, La Trobe University, Melbourne, VIC, Australia.
W ChenLa Trobe Institute for Molecular Science, La Trobe University, Melbourne, VIC, Australia.ORCID http://orcid.org/0000-0002-5221-9771
R D O'SheaDepartment of Physiology, Anatomy and Microbiology, School of Life Sciences, La Trobe University, Melbourne, VIC, Australia.ORCID http://orcid.org/0000-0002-8178-8797
L M WakimDepartment of Microbiology and Immunology, University of Melbourne, at Peter Doherty Institute for Infection and Immunity, Melbourne, VIC, Australia.
J M CarrMicrobiology and Infectious Diseases, College of Medicine and Public Health, Flinders University, Adelaide, SA, Australia.ORCID http://orcid.org/0000-0002-1080-1472
D R WhelanLa Trobe Institute for Molecular Science, La Trobe University, Melbourne, VIC, Australia.
K J HelbigDepartment of Physiology, Anatomy and Microbiology, School of Life Sciences, La Trobe University, Melbourne, VIC, Australia. k.helbig@latrobe.edu.au.ORCID http://orcid.org/0000-0001-6306-2821
La Trobe University · AUFlinders University · AUThe University of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lipid droplets (LDs) are increasingly recognized as critical organelles in signalling events, transient protein sequestration and inter-organelle interactions. However, the role LDs play in antiviral innate immune pathways remains unknown. Here we demonstrate that induction of LDs occurs as early as 2 h post-viral infection, is transient and returns to basal levels by 72 h. This phenomenon occurs following viral infections, both in vitro and in vivo. Virally driven in vitro LD induction is type-I interferon (IFN) independent, and dependent on Epidermal Growth Factor Receptor (EGFR) engagement, offering an alternate mechanism of LD induction in comparison to our traditional understanding of their biogenesis. Additionally, LD induction corresponds with enhanced cellular type-I and -III IFN production in infected cells, with enhanced LD accumulation decreasing viral replication of both Herpes Simplex virus 1 (HSV-1) and Zika virus (ZIKV). Here, we demonstrate, that LDs play vital roles in facilitating the magnitude of the early antiviral immune response specifically through the enhanced modulation of IFN following viral infection, and control of viral replication. By identifying LDs as a critical signalling organelle, this data represents a paradigm shift in our understanding of the molecular mechanisms which coordinate an effective antiviral response.

Indexed as

AnimalsErbB ReceptorsHerpesvirus 1, HumanHumansImmunity, InnateInterferonsLipid DropletsMiceNucleic AcidsVirus DiseasesVirus ReplicationZika VirusErbB ReceptorsInterferonsNucleic Acids

Identifiers

PMID34262037
PMCPMC8280141
OpenAlexW3178295484

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.