Evidence map›Paper›PMID 21533073›Full record

ArticlePLoS pathogens2011

Respiratory syncytial virus interferon antagonist NS1 protein suppresses and skews the human T lymphocyte response.

Shirin Munir, Philippa Hillyer, Cyril Le Nouën, Ursula J Buchholz, Ronald L Rabin, Peter L Collins, Alexander Bukreyev

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
7.8field-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

77 citing papers in PubMed, 124 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
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  5. Article
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  7. Article
  8. Review
  9. RSV: an overview of infection in adults.Pneumonia (Nathan Qld.) · 2025
    Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Dynamical Differences in Respiratory Syncytial Virus.Bulletin of mathematical biology · 2021
    Article
  17. Review
  18. Article
  19. Structural basis for IFN antagonism by human respiratory syncytial virus nonstructural protein 2.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  20. Review

17 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

7 authors at 3 institutions in 1 country.

Shirin MunirLaboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Philippa Hillyer
Cyril Le Nouën
Ursula J Buchholz
Ronald L Rabin
Peter L Collins
Alexander Bukreyev
National Institute of Allergy and Infectious Diseases · USCenter for Biologics Evaluation and Research · USNational Institutes of Health · US

Funding

Laboratory Studies of Human Respiratory Syncytial Virus and Other PneumovirusesZIAAI000372 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI BUCHHOLZ, URSULA · 2009 to 2025
$21.8M
Intramural NIH HHS
6 · The paper itself

Abstract

We recently demonstrated that the respiratory syncytial virus (RSV) NS1 protein, an antagonist of host type I interferon (IFN-I) production and signaling, has a suppressive effect on the maturation of human dendritic cells (DC) that was only partly dependent on released IFN-I. Here we investigated whether NS1 affects the ability of DC to activate CD8+ and CD4+ T cells. Human DC were infected with RSV deletion mutants lacking the NS1 and/or NS2 genes and assayed for the ability to activate autologous T cells in vitro, which were analyzed by multi-color flow cytometry. Deletion of the NS1, but not NS2, protein resulted in three major effects: (i) an increased activation and proliferation of CD8+ T cells that express CD103, a tissue homing integrin that directs CD8+ T cells to mucosal epithelial cells of the respiratory tract and triggers cytolytic activity; (ii) an increased activation and proliferation of Th17 cells, which have recently been shown to have anti-viral effects and also indirectly attract neutrophils; and (iii) decreased activation of IL-4-producing CD4+ T cells--which are associated with enhanced RSV disease--and reduced proliferation of total CD4+ T cells. Except for total CD4+ T cell proliferation, none of the T cell effects appeared to be due to increased IFN-I signaling. In the infected DC, deletion of the NS1 and NS2 genes strongly up-regulated the expression of cytokines and other molecules involved in DC maturation. This was partly IFN-I-independent, and thus might account for the T cell effects. Taken together, these data demonstrate that the NS1 protein suppresses proliferation and activation of two of the protective cell populations (CD103+ CD8+ T cells and Th17 cells), and promotes proliferation and activation of Th2 cells that can enhance RSV disease.

Indexed as

AdultAntigens, CDCell ProliferationCytokinesDendritic CellsFemaleHumansIntegrin alpha ChainsInterferonsMaleRespiratory Syncytial VirusesRespiratory Syncytial Virus InfectionsT-LymphocytesUp-RegulationViral Nonstructural Proteinsalpha E integrinsAntigens, CDCytokinesIntegrin alpha ChainsInterferonsViral Nonstructural Proteins

Identifiers

PMID21533073
PMCPMC3080852
OpenAlexW2063875739

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.