Evidence map›Paper›PMID 20660196›Full record

ArticleJournal of virology2010

Inhibition of the type I interferon response in human dendritic cells by dengue virus infection requires a catalytically active NS2B3 complex.

Juan R Rodriguez-Madoz, Alan Belicha-Villanueva, Dabeiba Bernal-Rubio, Joseph Ashour, Juan Ayllon, Ana Fernandez-Sesma

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed
11.5field-weighted citation impact, top 1% 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

90 citing papers in PubMed, 141 citations in OpenAlex.

  1. Article
  2. Dengue Dilemma: Navigating Cross-Reactivity and Immune Challenges.Current topics in microbiology and immunology · 2026
    Review
  3. Article
  4. Article
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  7. Review
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  20. Article

30 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

6 authors at 1 institution in 1 country.

Juan R Rodriguez-MadozDepartment of Microbiology, Mount Sinai School of Medicine, One Gustave L. Levy Place, Box 1124, New York, NY 10029, USA.
Alan Belicha-Villanueva
Dabeiba Bernal-Rubio
Joseph Ashour
Juan Ayllon
Ana Fernandez-Sesma
Icahn School of Medicine at Mount Sinai · US

Funding

MODULATION OF INNATE AND ADAPTIVE IMMUNITY BY DENGUE VIRUSR01AI073450 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI FERNANDEZ-SESMA, ANA · 2008 to 2017
$3.3M
NIAID NIH HHS 1R01AI073450NIAID NIH HHS R01 AI073450
6 · The paper itself

Abstract

Dengue virus (DENV) is the most prevalent arthropod-borne human virus, able to infect and replicate in human dendritic cells (DCs), inducing their activation and the production of proinflammatory cytokines. However, DENV can successfully evade the immune response in order to produce disease in humans. Several mechanisms of immune evasion have been suggested for DENV, most of them involving interference with type I interferon (IFN) signaling. We recently reported that DENV infection of human DCs does not induce type I IFN production by those infected DCs, impairing their ability to prime naive T cells toward Th1 immunity. In this article, we report that DENV also reduces the ability of DCs to produce type I IFN in response to several inducers, such as infection with other viruses or exposure to Toll-like receptor (TLR) ligands, indicating that DENV antagonizes the type I IFN production pathway in human DCs. DENV-infected human DCs showed a reduced type I IFN response to Newcastle disease virus (NDV), Sendai virus (SeV), and Semliki Forest virus (SFV) infection and to the TLR3 agonist poly(I:C). This inhibitory effect is DENV dose dependent, requires DENV replication, and takes place in DENV-infected DCs as early as 2 h after infection. Expressing individual proteins of DENV in the presence of an IFN-alpha/beta production inducer reveals that a catalytically active viral protease complex is required to reduce type I IFN production significantly. These results provide a new mechanism by which DENV evades the immune system in humans.

Indexed as

Immune EvasionAnimalsBase SequenceCell LineDendritic CellsDengue VirusDNA PrimersDogsHumansInterferon Type IIn Vitro TechniquesNewcastle disease virusSemliki forest virusSendai virusSignal TransductionT-LymphocytesDNA PrimersInterferon Type INS2B protein, flavivirusToll-Like ReceptorsViral Nonstructural Proteins

Identifiers

PMID20660196
PMCPMC2937777
OpenAlexW2037599622

What OpenQuestion holds

Textmetadata
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.