Evidence map›Paper›PMID 32449994›Full record

ArticleGlia2020

Microglia influence host defense, disease, and repair following murine coronavirus infection of the central nervous system.

Vrushali Mangale, Amber R Syage, H Atakan Ekiz, Dominic D Skinner, Yuting Cheng, Colleen L Stone, R Marshall Brown, Ryan M O'Connell, Kim N Green, Thomas E Lane

Open access · hybridAbstract read
In one paragraph

Article in Glia, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

50 citing papers in PubMed, 70 citations in OpenAlex.

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  9. Advances in Single-Cell Sequencing for Infectious Diseases: Progress and Perspectives.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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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

10 authors at 2 institutions in 1 country.

Vrushali MangaleDivision of Microbiology & Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, Utah, USA.
Amber R SyageDepartment of Neurobiology & Behavior, School of Biological Sciences, University of California, Irvine, California, USA.
H Atakan EkizDivision of Microbiology & Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, Utah, USA.
Dominic D SkinnerDivision of Microbiology & Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, Utah, USA.
Yuting ChengDepartment of Neurobiology & Behavior, School of Biological Sciences, University of California, Irvine, California, USA.
Colleen L StoneDivision of Microbiology & Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, Utah, USA.
R Marshall BrownDivision of Microbiology & Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, Utah, USA.
Ryan M O'ConnellDivision of Microbiology & Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, Utah, USA.
Kim N GreenDepartment of Neurobiology & Behavior, School of Biological Sciences, University of California, Irvine, California, USA.ORCID 0000-0002-6049-6744
Thomas E LaneDepartment of Neurobiology & Behavior, School of Biological Sciences, University of California, Irvine, California, USA.ORCID 0000-0003-0392-0825
University of Utah · USUniversity of California, Irvine · US

Funding

Utah Center for Clinical and Translational ScienceUL1TR002538 · NCATS · UNIVERSITY OF UTAH · PI HESS, RACHEL, MAJERSIK, JENNIFER JUHL · 2018 to 2022
$26.0M
Origins, properties, and therapeutic potential of cells that repopulate the microglia-depleted adult brainR01NS083801 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI Kim Green · 2014 to 2026
$5.6M
Chemokines and Viral-Induced Neurologic DiseaseR01NS041249 · NINDS · UNIVERSITY OF UTAH · PI LANE, THOMAS E · 2002 to 2019
$5.4M
Defining mechanisms of disease and repair in a viral model of multiple sclerosisR35NS116835 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI Thomas E Lane · 2020 to 2026
$5.0M
Viral-induced axonopathy: mechanisms of damage and repairR01NS091939 · NINDS · UNIVERSITY OF UTAH · PI FUJINAMI, ROBERT S, LANE, THOMAS E · 2016 to 2020
$1.7M
Micro RNAs and chronic, low-grade inflammationR01AG047956 · NIA · UNIVERSITY OF UTAH · PI O'CONNELL, RYAN M · 2015 to 2019
$1.7M
NCATS NIH HHS UL1 TR002538NIA NIH HHS R01 AG047956NIH HHS R01AG047956NINDS NIH HHS R01 NS041249NINDS NIH HHS R01NS041249NINDS NIH HHS R01 NS083801NINDS NIH HHS R01 NS091939NINDS NIH HHS R01NS091939NINDS NIH HHS R35 NS116835
6 · The paper itself

Abstract

The present study examines functional contributions of microglia in host defense, demyelination, and remyelination following infection of susceptible mice with a neurotropic coronavirus. Treatment with PLX5622, an inhibitor of colony stimulating factor 1 receptor (CSF1R) that efficiently depletes microglia, prior to infection of the central nervous system (CNS) with the neurotropic JHM strain of mouse hepatitis virus (JHMV) resulted in increased mortality compared with control mice that correlated with impaired control of viral replication. Single cell RNA sequencing (scRNASeq) of CD45+ cells isolated from the CNS revealed that PLX5622 treatment resulted in muted CD4+ T cell activation profile that was associated with decreased expression of transcripts encoding MHC class II and CD86 in macrophages but not dendritic cells. Evaluation of spinal cord demyelination revealed a marked increase in white matter damage in PLX5622-treated mice that corresponded with elevated expression of transcripts encoding disease-associated proteins Osteopontin (Spp1), Apolipoprotein E (Apoe), and Triggering receptor expressed on myeloid cells 2 (Trem2) that were enriched within macrophages. In addition, PLX5622 treatment dampened expression of Cystatin F (Cst7), Insulin growth factor 1 (Igf1), and lipoprotein lipase (Lpl) within macrophage populations which have been implicated in promoting repair of damaged nerve tissue and this was associated with impaired remyelination. Collectively, these findings argue that microglia tailor the CNS microenvironment to enhance control of coronavirus replication as well as dampen the severity of demyelination and influence repair.

Indexed as

AnimalsBrainCoronavirus InfectionsHost-Pathogen InteractionsImmunity, CellularMaleMiceMice, Inbred C57BLMicrogliaMurine hepatitis virusOrganic ChemicalsOrganic ChemicalsPLX5622coronavirusdemyelinationhost defensemicrogliaremyelination

Identifiers

PMID32449994
PMCPMC7280614
OpenAlexW3028688943

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.