Evidence map›Paper›PMID 23094089›Full record

ArticlePloS one2012

Distinct and overlapping roles of Nipah virus P gene products in modulating the human endothelial cell antiviral response.

Michael K Lo, Mark E Peeples, William J Bellini, Stuart T Nichol, Paul A Rota, Christina F Spiropoulou

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

37 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
  2. Article
  3. Nipah virus: a summary for clinicians.International journal of emergency medicine · 2025
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Recombinant Cedar Virus: A Henipavirus Reverse Genetics Platform.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Inhibition of Nipah Virus by Defective Interfering Particles.The Journal of infectious diseases · 2020
    Article
  16. Article
  17. Article
  18. Article
  19. Nano-based approach to combat emerging viral (NIPAH virus) infection.Nanomedicine : nanotechnology, biology, and medicine · 2019
    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

6 authors at 3 institutions in 1 country.

Michael K LoCenters for Disease Control & Prevention, Viral Special Pathogens Branch, Atlanta, Georgia, United States of America. mko2@cdc.gov
Mark E Peeples
William J Bellini
Stuart T Nichol
Paul A Rota
Christina F Spiropoulou
Centers for Disease Control and Prevention · USThe Centers · USThe Ohio State University · US

Funding

Respiratory Syncytial Virus Targeting of the Human Airway EpitheliumR01AI093848 · NIAID · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI PEEPLES, MARK E. · 2012 to 2023
$3.8M
Generation of a Single-Cycle Virus to Study the Pathogenesis of Nipah VirusR21AI069014 · NIAID · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI PEEPLES, MARK E. · 2006 to 2007
$384k
NIAID NIH HHS AI069014NIAID NIH HHS R01 AI093848NIAID NIH HHS R21 AI069014
6 · The paper itself

Abstract

Nipah virus (NiV) is a highly pathogenic zoonotic paramyxovirus that causes fatal encephalitis in up to 75% of infected humans. Like other paramyxoviruses, NiV employs co-transcriptional mRNA editing during transcription of the phosphoprotein (P) gene to generate additional mRNAs encoding the V and W proteins. The C protein is translated from the P mRNA, but in an alternative reading frame. There is evidence from both in vitro and in vivo studies to show that the P gene products play a role in NiV pathogenesis. We have developed a reverse genetic system to dissect the individual roles of the NiV P gene products in limiting the antiviral response in primary human microvascular lung endothelial cells, which represent important targets in human NiV infection. By characterizing growth curves and early antiviral responses against a number of recombinant NiVs with genetic modifications altering expression of the proteins encoded by the P gene, we observed that multiple elements encoded by the P gene have both distinct and overlapping roles in modulating virus replication as well as in limiting expression of antiviral mediators such as IFN-β, CXCL10, and CCL5. Our findings corroborate observations from in vivo hamster infection studies, and provide molecular insights into the attenuation and the histopathology observed in hamsters infected with C, V, and W-deficient NiVs. The results of this study also provide an opportunity to verify the results of earlier artificial plasmid expression studies in the context of authentic viral infection.

Indexed as

Gene Expression Regulation, ViralCell LineChemokine CCL5Chemokine CXCL10Endothelial CellsEndothelium, VascularHenipavirus InfectionsHost-Pathogen InteractionsHumansInterferon-betaNipah VirusPhosphoproteinsPrimary Cell CultureReverse GeneticsRNA, MessengerRNA, ViralCCL5 protein, humanChemokine CCL5Chemokine CXCL10CXCL10 protein, humanInterferon-betaPhosphoproteinsRNA, MessengerRNA, ViralViral Proteins

Identifiers

PMID23094089
PMCPMC3477106
OpenAlexW1969126808

What OpenQuestion holds

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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.