Evidence map›Paper›PMID 29377936›Full record

ArticlePLoS pathogens2018

Alphavirus-induced hyperactivation of PI3K/AKT directs pro-viral metabolic changes.

Michela Mazzon, Cecilia Castro, Bastian Thaa, Lifeng Liu, Margit Mutso, Xiang Liu, Suresh Mahalingam, Julian L Griffin, Mark Marsh, Gerald M McInerney

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
9.4field-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

46 citing papers in PubMed, 63 citations in OpenAlex.

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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 4 institutions in 4 countries.

Michela MazzonMRC Laboratory for Molecular Cell Biology, University College London, London, United Kingdom.ORCID 0000-0002-2462-9925
Cecilia CastroDepartment of Biochemistry, University of Cambridge, Cambridge, United Kingdom.
Bastian ThaaDepartment of Microbiology, Tumor and Cell Biology (MTC), Karolinska Institutet, Stockholm, SE, Sweden.ORCID 0000-0001-8800-9584
Lifeng LiuDepartment of Microbiology, Tumor and Cell Biology (MTC), Karolinska Institutet, Stockholm, SE, Sweden.
Margit MutsoInstitute of Glycomics, Griffith University, Gold Coast, Queensland, Australia.
Xiang LiuInstitute of Glycomics, Griffith University, Gold Coast, Queensland, Australia.
Suresh MahalingamInstitute of Glycomics, Griffith University, Gold Coast, Queensland, Australia.ORCID 0000-0003-3141-8410
Julian L GriffinDepartment of Biochemistry, University of Cambridge, Cambridge, United Kingdom.ORCID 0000-0003-1336-7744
Mark MarshMRC Laboratory for Molecular Cell Biology, University College London, London, United Kingdom.ORCID 0000-0002-0213-3259
Gerald M McInerneyDepartment of Microbiology, Tumor and Cell Biology (MTC), Karolinska Institutet, Stockholm, SE, Sweden.ORCID 0000-0003-2257-7241
Griffith University · AUKarolinska Institutet · SEMRC Laboratory for Molecular Cell Biology · GBUniversity of Cambridge · GB

Funding

Medical Research Council MC_UP_A090_1006Medical Research Council MC_UU_00012/1Medical Research Council MC_UU_12018/1Medical Research Council MR/K015826/1Medical Research Council MR/P011705/1Wellcome Trust
6 · The paper itself

Abstract

Virus reprogramming of cellular metabolism is recognised as a critical determinant for viral growth. While most viruses appear to activate central energy metabolism, different viruses have been shown to rely on alternative mechanisms of metabolic activation. Whether related viruses exploit conserved mechanisms and induce similar metabolic changes is currently unclear. In this work we investigate how two alphaviruses, Semliki Forest virus and Ross River virus, reprogram host metabolism and define the molecular mechanisms responsible. We demonstrate that in both cases the presence of a YXXM motif in the viral protein nsP3 is necessary for binding to the PI3K regulatory subunit p85 and for activating AKT. This leads to an increase in glucose metabolism towards the synthesis of fatty acids, although additional mechanisms of metabolic activation appear to be involved in Ross River virus infection. Importantly, a Ross River virus mutant that fails to activate AKT has an attenuated phenotype in vivo, suggesting that viral activation of PI3K/AKT contributes to virulence and disease.

Indexed as

Host-Pathogen InteractionsAlphavirusAlphavirus InfectionsAnimalsCells, CulturedCricetinaeEnzyme ActivationGlucoseGlycolysisHEK293 CellsHumansMiceMice, Inbred C57BLPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRoss River virusGlucosePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID29377936
PMCPMC5805360
OpenAlexW2787348393

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.