Evidence map›Paper›PMID 39226332›Full record

ArticlePLoS pathogens2024

Norovirus-mediated translation repression promotes macrophage cell death.

Turgut E Aktepe, Joshua M Deerain, Jennifer L Hyde, Svenja Fritzlar, Eleanor M Mead, Julio Carrera Montoya, Abderrahman Hachani, Jaclyn S Pearson, Peter A White, Jason M Mackenzie

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PLoS pathogens, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. Article
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.

Turgut E AktepeDepartment of Microbiology and Immunology, at the Peter Doherty Institute for Infection and Immunity, University of Melbourne, Melbourne, Australia.
Joshua M DeerainDepartment of Microbiology and Immunology, at the Peter Doherty Institute for Infection and Immunity, University of Melbourne, Melbourne, Australia.
Jennifer L HydeDepartment of Microbiology, School of Medicine, University of Washington, Seattle, Washington, United States of America.
Svenja FritzlarDepartment of Microbiology and Immunology, at the Peter Doherty Institute for Infection and Immunity, University of Melbourne, Melbourne, Australia.
Eleanor M MeadDepartment of Microbiology and Immunology, at the Peter Doherty Institute for Infection and Immunity, University of Melbourne, Melbourne, Australia.
Julio Carrera MontoyaDepartment of Microbiology and Immunology, at the Peter Doherty Institute for Infection and Immunity, University of Melbourne, Melbourne, Australia.
Abderrahman HachaniDepartment of Microbiology and Immunology, at the Peter Doherty Institute for Infection and Immunity, University of Melbourne, Melbourne, Australia.
Jaclyn S PearsonThe Hudson Institute of Medical Research, Centre for Innate Immunity and Infectious Diseases, Melbourne, Australia.
Peter A WhiteSchool of Biotechnology and Biomolecular Sciences, University of New South Wales, Sydney, Australia.
Jason M MackenzieDepartment of Microbiology and Immunology, at the Peter Doherty Institute for Infection and Immunity, University of Melbourne, Melbourne, Australia.ORCID 0000-0001-6613-8350

Funding

National Health and Medical Research Council of Australia 1123135The Miller FoundationUniversity of Melbourne
6 · The paper itself

Abstract

Norovirus infection is characterised by a rapid onset of disease and the development of debilitating symptoms including projectile vomiting and diffuse diarrhoea. Vaccines and antivirals are sorely lacking and developments in these areas are hampered by the lack of an adequate cell culture system to investigate human norovirus replication and pathogenesis. Herein, we describe how the model norovirus, Mouse norovirus (MNV), produces a viral protein, NS3, with the functional capacity to attenuate host protein translation which invokes the activation of cell death via apoptosis. We show that this function of NS3 is conserved between human and mouse viruses and map the protein domain attributable to this function. Our study highlights a critical viral protein that mediates crucial activities during replication, potentially identifying NS3 as a worthy target for antiviral drug development.

Indexed as

Caliciviridae InfectionsMacrophagesNorovirusAnimalsApoptosisCell DeathHumansMiceProtein BiosynthesisViral Nonstructural ProteinsVirus ReplicationViral Nonstructural Proteins

Identifiers

PMID39226332
PMCPMC11398682

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.