Evidence map›Paper›PMID 30001425›Full record

ArticlePLoS pathogens2018

DDX3 suppresses type I interferons and favors viral replication during Arenavirus infection.

María Eugenia Loureiro, Andre Luiz Zorzetto-Fernandes, Sheli Radoshitzky, Xiaoli Chi, Simone Dallari, Nuha Marooki, Psylvia Lèger, Sabrina Foscaldi, Vince Harjono, Sonia Sharma and 5 more

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 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

32 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. A Dual Role of DDX3X in dsRNA-Derived Innate Immune Signaling.Frontiers in molecular biosciences · 2022
    Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. 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

15 authors at 5 institutions in 2 countries.

María Eugenia LoureiroDivision of Biological Sciences, University of California San Diego, La Jolla, CA, United States of America.ORCID 0000-0001-7965-0177
Andre Luiz Zorzetto-FernandesDivision of Biological Sciences, University of California San Diego, La Jolla, CA, United States of America.ORCID 0000-0002-1740-4402
Sheli RadoshitzkyMolecular and Translational Sciences Division, United States Army Medical Research Institute of Infectious Diseases, Frederick, MD, United States of America.
Xiaoli ChiMolecular and Translational Sciences Division, United States Army Medical Research Institute of Infectious Diseases, Frederick, MD, United States of America.
Simone DallariDivision of Biological Sciences, University of California San Diego, La Jolla, CA, United States of America.
Nuha MarookiDivision of Biological Sciences, University of California San Diego, La Jolla, CA, United States of America.
Psylvia LègerDivision of Biological Sciences, University of California San Diego, La Jolla, CA, United States of America.ORCID 0000-0001-7148-7125
Sabrina FoscaldiCentro de Virología Animal, Consejo Nacional de Investigaciones Científicas y Técnicas, Buenos Aires, Argentina.ORCID 0000-0002-3502-0859
Vince HarjonoDepartment of Chemistry and Biochemistry, University of California San Diego, La Jolla, CA, United States of America.ORCID 0000-0002-3433-4629
Sonia SharmaLa Jolla Institute for Allergy and Immunology, La Jolla, CA, United States of America.
Brian M ZidDepartment of Chemistry and Biochemistry, University of California San Diego, La Jolla, CA, United States of America.ORCID 0000-0003-1876-2479
Nora LópezCentro de Virología Animal, Consejo Nacional de Investigaciones Científicas y Técnicas, Buenos Aires, Argentina.ORCID 0000-0001-9782-9330
Juan Carlos de la TorreThe Scripps Research Institute, Department of Immunology and Microbiology, La Jolla, CA, United States of America.
Sina BavariMolecular and Translational Sciences Division, United States Army Medical Research Institute of Infectious Diseases, Frederick, MD, United States of America.
Elina ZúñigaDivision of Biological Sciences, University of California San Diego, La Jolla, CA, United States of America.
University of California San Diego · USUnited States Army Medical Research Institute of Infectious Diseases · USConsejo Nacional de Investigaciones Científicas y Técnicas · ARLa Jolla Institute for Immunology · USScripps Research Institute · US

Funding

GENETIC MECHANISMS AND REGULATIONT32GM007240 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HAMPTON, RANDOLPH Y. · 1985 to 2019
$23.8M
U of Calif, San Diego Neuroscience Microscopy ImagingP30NS047101 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GLEESON, JOSEPH G, ZHENG, BINHAI · 2003 to 2022
$9.0M
Inhibitory Pathways Underlying Viral Persistence In VivoR01AI081923 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Elina I Zuniga · 2009 to 2026
$6.6M
Positive Immune-regulators During Chronic Viral InfectionsR01AI113923 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ZUNIGA, ELINA I · 2015 to 2024
$5.1M
Targeting tumor endothelium for cancer surveillance and immunotherapyR01CA199376 · NCI · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI SHARMA, SONIA · 2015 to 2019
$2.0M
NCI NIH HHS R01 CA199376NIAID NIH HHS R01 AI081923NIAID NIH HHS R01 AI113923NIGMS NIH HHS T32 GM007240NINDS NIH HHS P30 NS047101
6 · The paper itself

Abstract

Several arenaviruses cause hemorrhagic fever (HF) diseases that are associated with high morbidity and mortality in humans. Accordingly, HF arenaviruses have been listed as top-priority emerging diseases for which countermeasures are urgently needed. Because arenavirus nucleoprotein (NP) plays critical roles in both virus multiplication and immune-evasion, we used an unbiased proteomic approach to identify NP-interacting proteins in human cells. DDX3, a DEAD-box ATP-dependent-RNA-helicase, interacted with NP in both NP-transfected and virus-infected cells. Importantly, DDX3 deficiency compromised the propagation of both Old and New World arenaviruses, including the HF arenaviruses Lassa and Junin viruses. The DDX3 role in promoting arenavirus multiplication associated with both a previously un-recognized DDX3 inhibitory role in type I interferon production in arenavirus infected cells and a positive DDX3 effect on arenavirus RNA synthesis that was dependent on its ATPase and Helicase activities. Our results uncover novel mechanisms used by arenaviruses to exploit the host machinery and subvert immunity, singling out DDX3 as a potential host target for developing new therapies against highly pathogenic arenaviruses.

Indexed as

Arenaviridae InfectionsArenavirusCell LineDEAD-box RNA HelicasesHost-Pathogen InteractionsHumansImmune EvasionInterferon Type IViral Core ProteinsVirus ReplicationDDX3X protein, humanDEAD-box RNA HelicasesInterferon Type IViral Core Proteins

Identifiers

PMID30001425
PMCPMC6042795
OpenAlexW2817795281

What OpenQuestion holds

Textmetadata
LicenceCC0
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.