Evidence map›Paper›PMID 30862747›Full record

ArticlemBio2019

Glycolysis Is an Intrinsic Factor for Optimal Replication of a Norovirus.

Karla D Passalacqua, Jia Lu, Ian Goodfellow, Abimbola O Kolawole, Jacob R Arche, Robert J Maddox, Kelly E Carnahan, Mary X D O'Riordan, Christiane E Wobus

Open access · goldAbstract read
In one paragraph

Article in mBio, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
7.8field-weighted citation impact, top 2% 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

63 citing papers in PubMed, 96 citations in OpenAlex.

  1. Article
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  5. The return of metabolism: biochemistry and physiology of glycolysis.Biological reviews of the Cambridge Philosophical Society · 2026
    Review
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  16. Glucose-independent human cytomegalovirus replication is supported by metabolites that feed upper glycolytic branches.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
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3 more citing papers are in PubMed but not listed here.

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

9 authors at 2 institutions in 2 countries.

Karla D PassalacquaDepartment of Microbiology and Immunology, University of Michigan, Ann Arbor, Michigan, USA.
Jia LuDivision of Virology, Department of Pathology, University of Cambridge, Cambridge, United Kingdom.
Ian GoodfellowDivision of Virology, Department of Pathology, University of Cambridge, Cambridge, United Kingdom.
Abimbola O KolawoleDepartment of Microbiology and Immunology, University of Michigan, Ann Arbor, Michigan, USA.
Jacob R ArcheDepartment of Microbiology and Immunology, University of Michigan, Ann Arbor, Michigan, USA.
Robert J MaddoxDepartment of Microbiology and Immunology, University of Michigan, Ann Arbor, Michigan, USA.
Kelly E CarnahanDepartment of Microbiology and Immunology, University of Michigan, Ann Arbor, Michigan, USA.
Mary X D O'RiordanDepartment of Microbiology and Immunology, University of Michigan, Ann Arbor, Michigan, USA.
Christiane E WobusDepartment of Microbiology and Immunology, University of Michigan, Ann Arbor, Michigan, USA cwobus@umich.edu.ORCID 0000-0001-5286-0924
University of Michigan · USUniversity of Cambridge · GB

Funding

Statistics and Bioinformatics Core - WangU24DK097153 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BURANT, CHARLES F · 2012 to 2017
$10.1M
Targeting host deubiquitinases for broad spectrum anti-infective therapyR33AI102106 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI O'RIORDAN, MARY · 2014 to 2016
$1.4M
Targeting host deubiquitinases for broad spectrum anti-infective therapyR21AI102106 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI O'RIORDAN, MARY, WOBUS, CHRISTIANE · 2012 to 2013
$423k
Biotechnology and Biological Sciences Research Council BB/N001176/1NIAID NIH HHS R21 AI102106NIAID NIH HHS R33 AI102106NIDDK NIH HHS U24 DK097153Wellcome TrustWellcome Trust 207498/Z/17/Z
6 · The paper itself

Abstract

The metabolic pathways of central carbon metabolism, glycolysis and oxidative phosphorylation (OXPHOS), are important host factors that determine the outcome of viral infections and can be manipulated by some viruses to favor infection. However, mechanisms of metabolic modulation and their effects on viral replication vary widely. Herein, we present the first metabolomics and energetic profiling of norovirus-infected cells, which revealed increases in glycolysis, OXPHOS, and the pentose phosphate pathway (PPP) during murine norovirus (MNV) infection. Inhibiting glycolysis with 2-deoxyglucose (2DG) in macrophages revealed that glycolysis is an important factor for optimal MNV infection, while inhibiting the PPP and OXPHOS showed a relatively minor impact of these pathways on MNV infection. 2DG affected an early stage in the viral life cycle after viral uptake and capsid uncoating, leading to decreased viral protein production and viral RNA. The requirement of glycolysis was specific for MNV (but not astrovirus) infection, independent of the type I interferon antiviral response, and unlikely to be due to a lack of host cell nucleotide synthesis. MNV infection increased activation of the protein kinase Akt, but not AMP-activated protein kinase (AMPK), two master regulators of cellular metabolism, implicating Akt signaling in upregulating host metabolism during norovirus infection. In conclusion, our findings suggest that the metabolic state of target cells is an intrinsic host factor that determines the extent of norovirus replication and implicates glycolysis as a virulence determinant. They further point to cellular metabolism as a novel therapeutic target for norovirus infections and improvements in current human norovirus culture systems.

Indexed as

GlycolysisHost-Pathogen InteractionsVirus ReplicationAnimalsCaco-2 CellsCaliciviridae InfectionsHumansMacrophagesMetabolomicsMiceNorovirusOxidative PhosphorylationPentose Phosphate PathwayRAW 264.7 Cellscaliciviruscarbon metabolismglycolysisnorovirusesoxidative phosphorylationpentose phosphate pathway

Identifiers

PMID30862747
PMCPMC6414699
OpenAlexW2921137413

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.