Evidence map›Paper›PMID 26764599›Full record

ArticleCell host & microbe2016

Autophagy Genes Enhance Murine Gammaherpesvirus 68 Reactivation from Latency by Preventing Virus-Induced Systemic Inflammation.

Sunmin Park, Michael D Buck, Chandni Desai, Xin Zhang, Ekaterina Loginicheva, Jennifer Martinez, Michael L Freeman, Tatsuya Saitoh, Shizuo Akira, Jun-Lin Guan and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell host & microbe, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing 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

48 citing papers in PubMed, 58 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors at 11 institutions in 2 countries.

Sunmin ParkDepartment of Pathology and Immunology, Washington University in St. Louis, St. Louis, MO 63110, USA.
Michael D BuckDepartment of Pathology and Immunology, Washington University in St. Louis, St. Louis, MO 63110, USA.
Chandni DesaiDepartment of Pathology and Immunology, Washington University in St. Louis, St. Louis, MO 63110, USA.
Xin ZhangDepartment of Pathology and Immunology, Washington University in St. Louis, St. Louis, MO 63110, USA.
Ekaterina LoginichevaDepartment of Pathology and Immunology, Washington University in St. Louis, St. Louis, MO 63110, USA.
Jennifer MartinezImmunity, Inflammation, and Disease Laboratory, NIEHS, National Institutes of Health, Research Triangle Park, NC 27703, USA.
Michael L FreemanDivision of Infectious Diseases, Case Western Reserve University, Cleveland, OH 44106, USA.
Tatsuya SaitohDivision of Molecular Genetics, Institute for Enzyme Research, Tokushima University, 3-8-15 Kuramoto-cho, Tokushima 770-8503, Japan.
Shizuo AkiraDepartment of Host Defense, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan.
Jun-Lin GuanDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
You-Wen HeDepartment of Immunology, Duke University Medical Center, Durham, NC 27710, USA.
Marcia A BlackmanTrudeau Institute, Saranac Lake, NY 12983, USA.
Scott A HandleyDepartment of Pathology and Immunology, Washington University in St. Louis, St. Louis, MO 63110, USA.
Beth LevineCenter for Autophagy Research, Department of Internal Medicine and Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Douglas R GreenDepartment of Immunology, St Jude Children's Research Hospital, Memphis, TN 38105, USA.
Tiffany A ReeseDepartment of Immunology and Microbiology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Maxim N ArtyomovDepartment of Pathology and Immunology, Washington University in St. Louis, St. Louis, MO 63110, USA.
Herbert W VirginDepartment of Pathology and Immunology, Washington University in St. Louis, St. Louis, MO 63110, USA. Electronic address: virgin@wustl.edu.
Washington University in St. Louis · USCase Western Reserve University · USDuke Medical Center · USHoward Hughes Medical Institute · USNational Institutes of Health · USSt. Jude Children's Research Hospital · USThe University of Osaka · JPThe University of Texas Southwestern Medical Center · USTokushima University · JPTrudeau Institute · USUniversity of Cincinnati Medical Center · US

Funding

Genetic and Pathway Analysis CoreU19AI109725 · NIAID · WASHINGTON UNIVERSITY · PI ALLEN, PAUL M · 2014 to 2018
$32.7M
Washington University DDRCC Supplemental Equipment RequestP30DK052574 · NIDDK · WASHINGTON UNIVERSITY · PI Nicholas O. Davidson · 2000 to 2026
$30.8M
Characterization of the molecular mechanisms of LC3-associated phagocytosis and its role in disease pathogenesisZIAES103286 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI MARTINEZ, JENNIFER · 2015 to 2021
$9.2M
Viral Discovery in Rheumatoid ArthritisP30AR048335 · NIAMS · WASHINGTON UNIVERSITY · PI WEIHL, CONRAD C · 2001 to 2015
$8.9M
Non-canonical functions of autophagy proteinsR01AI040646 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI GREEN, DOUGLAS R. · 1997 to 2023
$8.6M
Intramural NIH HHS Z99 ES999999Intramural NIH HHS ZIA ES103286NIAID NIH HHS R01 AI040646NIAID NIH HHS U19 AI109725NIAID NIH HHS U19AI109725NIAMS NIH HHS NIH P30AR048335NIAMS NIH HHS P30 AR048335NIDDK NIH HHS P30 DK052574
6 · The paper itself

Abstract

Host genes that regulate systemic inflammation upon chronic viral infection are incompletely understood. Murine gammaherpesvirus 68 (MHV68) infection is characterized by latency in macrophages, and reactivation is inhibited by interferon-γ (IFN-γ). Using a lysozyme-M-cre (LysMcre) expression system, we show that deletion of autophagy-related (Atg) genes Fip200, beclin 1, Atg14, Atg16l1, Atg7, Atg3, and Atg5, in the myeloid compartment, inhibited MHV68 reactivation in macrophages. Atg5 deficiency did not alter reactivation from B cells, and effects on reactivation from macrophages were not explained by alterations in productive viral replication or the establishment of latency. Rather, chronic MHV68 infection triggered increased systemic inflammation, increased T cell production of IFN-γ, and an IFN-γ-induced transcriptional signature in macrophages from Atg gene-deficient mice. The Atg5-related reactivation defect was partially reversed by neutralization of IFN-γ. Thus Atg genes in myeloid cells dampen virus-induced systemic inflammation, creating an environment that fosters efficient MHV68 reactivation from latency.

Indexed as

AutophagyVirus ActivationVirus LatencyAnimalsAutophagy-Related Protein 5Autophagy-Related Protein 7Autophagy-Related ProteinsHerpesviridae InfectionsHost-Pathogen InteractionsInterferon-gammaMiceMicrotubule-Associated ProteinsMyeloid CellsRhadinovirusUbiquitin-Conjugating EnzymesAtg3 protein, mouseAtg5 protein, mouseAtg7 protein, mouseAutophagy-Related Protein 5Autophagy-Related Protein 7Autophagy-Related ProteinsInterferon-gammaMicrotubule-Associated ProteinsUbiquitin-Conjugating Enzymes

Identifiers

PMID26764599
PMCPMC4714357
OpenAlexW2239321195

What OpenQuestion holds

Textmetadata
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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.