Evidence map›Paper›PMID 31534040›Full record

ArticleJournal of virology2019

West Nile Virus Infection Blocks Inflammatory Response and T Cell Costimulatory Capacity of Human Monocyte-Derived Dendritic Cells.

Matthew G Zimmerman, James R Bowen, Circe E McDonald, Bali Pulendran, Mehul S Suthar

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

19 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. West Nile virus unmasked: from gene variability to future challenges.Frontiers in cellular and infection microbiology · 2025
    Review
  6. Review
  7. Myeloid-Derived Suppressor Cells Induce Exhaustion-Like CD8International journal of biological sciences · 2024
    Article
  8. Article
  9. Review
  10. Article
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  12. Article
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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

5 authors at 1 institution in 1 country.

Matthew G Zimmerman *Department of Pediatrics, Division of Infectious Diseases, Emory University School of Medicine, Atlanta, Georgia, USA.
James R Bowen *Department of Pediatrics, Division of Infectious Diseases, Emory University School of Medicine, Atlanta, Georgia, USA.
Circe E McDonaldDepartment of Pediatrics, Division of Infectious Diseases, Emory University School of Medicine, Atlanta, Georgia, USA.
Bali PulendranEmory Vaccine Center, Yerkes National Primate Research Center, Atlanta, Georgia, USA.
Mehul S SutharDepartment of Pediatrics, Division of Infectious Diseases, Emory University School of Medicine, Atlanta, Georgia, USA msuthar@emory.edu.ORCID 0000-0002-2686-8380
Emory University · US

Funding

Yerkes National Primate Research Center Role of type-I IFN in regulating COVID-19 induced inflammation and pathogenesisP51OD011132 · OD · EMORY UNIVERSITY · PI Joon Sup Lee · 2012 to 2026
$167.0M
VACCINE INDUCED IMMUNITY IN THE YOUNG AND AGEDU19AI057266 · NIAID · EMORY UNIVERSITY · PI Rafi Ahmed · 2003 to 2026
$81.7M
Systems Biological Analysis of Innate and Adaptive Responses to VaccinationU19AI090023 · NIAID · EMORY UNIVERSITY · PI AHMED, RAFI, LI, SHUZHAO · 2010 to 2021
$45.0M
West Nile Virus and host control of innate defensesU19AI083019 · NIAID · UNIVERSITY OF WASHINGTON · PI CLARK, EDWARD A · 2009 to 2018
$22.5M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM008169 · NIGMS · EMORY UNIVERSITY · PI GROSS, ROBERT E · 1987 to 2021
$20.3M
MICROBES, DENDRITIC CELL SUBSETS AND T-CELL IMMUNITYR01AI048638 · NIAID · STANFORD UNIVERSITY · PI PULENDRAN, BALI · 2001 to 2024
$4.5M
Understanding the Role of Mucosal Antigen Presenting Cells in Regulating Immune ResponseR37AI048638 · NIAID · STANFORD UNIVERSITY · PI PULENDRAN, BALI · 2009 to 2018
$4.0M
Polarizing T Cell Responses in vivo With Dendritic CellsR37DK057665 · NIDDK · STANFORD UNIVERSITY · PI PULENDRAN, BALI · 2010 to 2019
$3.9M
Determining how macrophages regulate immunity to Zika virus infection at the maternal-fetal interfaceU01AI131566 · NIAID · EMORY UNIVERSITY · PI CHAKRABORTY, RANA, SUTHAR, MEHUL SHAMAL · 2017 to 2021
$2.3M
Identifying host genetic determinants that regulate dendritic cell activationR21AI113485 · NIAID · EMORY UNIVERSITY · PI SUTHAR, MEHUL SHAMAL · 2015 to 2016
$494k
Regulation of T cell immunity by the cytosolic RIG-I like receptorsR56AI110516 · NIAID · EMORY UNIVERSITY · PI SUTHAR, MEHUL SHAMAL · 2014 to 2014
$443k
Mechanisms by which trophoblasts recruit T cells to the placental villi during maternal HIV and CMV co-infectionR21HD103498 · NICHD · MAYO CLINIC ROCHESTER · PI CHAKRABORTY, RANA, GRAY, CLIVE MAURICE · 2020 to 2021
$390k
NIAID NIH HHS R01 AI048638NIAID NIH HHS R21 AI113485NIAID NIH HHS R37 AI048638NIAID NIH HHS R56 AI110516NIAID NIH HHS U01 AI131566NIAID NIH HHS U19 AI057266NIAID NIH HHS U19 AI083019NIAID NIH HHS U19 AI090023NICHD NIH HHS R21 HD103498NIDDK NIH HHS R37 DK057665NIGMS NIH HHS T32 GM008169NIH HHS P51 OD011132
6 · The paper itself

Abstract

West Nile virus (WNV) is a neurotropic flavivirus and the leading cause of mosquito-borne encephalitis in the United States. Recent studies in humans have found that dysfunctional T cell responses strongly correlate with development of severe WNV neuroinvasive disease. However, the contributions of human dendritic cells (DCs) in priming WNV-specific T cell immunity remains poorly understood. Here, we demonstrate that human monocyte derived DCs (moDCs) support productive viral replication following infection with a pathogenic strain of WNV. Antiviral effector gene transcription was strongly induced during the log phase of viral growth, while secretion of type I interferons (IFN) occurred with delayed kinetics. Activation of RIG-I like receptor (RLR) or type I IFN signaling prior to log phase viral growth significantly diminished viral replication, suggesting that early activation of antiviral programs can block WNV infection. In contrast to the induction of antiviral responses, WNV infection did not promote transcription or secretion of proinflammatory (interleukin-6 [IL-6], granulocyte-macrophage colony-stimulating factor [GM-CSF], CCL3, CCL5, and CXCL9) or T cell modulatory (IL-4, IL-12, and IL-15) cytokines. There was also minimal induction of molecules associated with antigen presentation and T cell priming, including the costimulatory molecules CD80, CD86, and CD40. Functionally, WNV-infected moDCs dampened allogenic CD4 and CD8 T cell activation and proliferation. Combining these observations, we propose a model whereby WNV subverts human DC activation to compromise priming of WNV-specific T cell immunity.

Indexed as

AnimalsAntiviral AgentsCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCell LineCell ProliferationChlorocebus aethiopsCytokinesDEAD Box Protein 58Dendritic CellsFlavivirusHumansImmunity, InnateInterferon Type ILymphocyte ActivationMonocytesAntiviral AgentsCytokinesDEAD Box Protein 58Interferon Type IReceptors, ImmunologicRIGI protein, humandendritic cellsRIG-I-like receptorstype I interferonWest Nile virus

Identifiers

PMID31534040
PMCPMC6854506
OpenAlexW2972635785

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.