Evidence map›Paper›PMID 31043529›Full record

ArticleJournal of virology2019

Chandipura Virus Utilizes the Prosurvival Function of RelA NF-κB for Its Propagation.

Sachendra S Bais, Yashika Ratra, Naseem A Khan, Rakesh Pandey, Pramod K Kushawaha, Shailly Tomar, Guruprasad Medigeshi, Abhyudai Singh, Soumen Basak

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 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
  5. Article
  6. Article
  7. IRF3 inhibits nuclear translocation of NF-κB to prevent viral inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
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  10. Review
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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

9 authors at 4 institutions in 2 countries.

Sachendra S BaisSystems Immunology Laboratory, National Institute of Immunology, New Delhi, India.
Yashika RatraSystems Immunology Laboratory, National Institute of Immunology, New Delhi, India.
Naseem A KhanTranslational Health Sciences and Technology Institute, Faridabad, India.
Rakesh PandeySystems Immunology Laboratory, National Institute of Immunology, New Delhi, India.
Pramod K KushawahaSystems Immunology Laboratory, National Institute of Immunology, New Delhi, India.
Shailly TomarDepartment of Biotechnology, Indian Institute of Technology, Roorkee, India.
Guruprasad MedigeshiTranslational Health Sciences and Technology Institute, Faridabad, India.ORCID 0000-0001-5333-9743
Abhyudai SinghBiomedical Engineering Department, University of Delaware, Newark, New Jersey, USA.
Soumen BasakSystems Immunology Laboratory, National Institute of Immunology, New Delhi, India sobasak@nii.ac.in.ORCID 0000-0002-3586-1279
National Institute of Immunology · INTranslational Health Science and Technology Institute · INIndian Institute of Technology Roorkee · INUniversity of Delaware · US

Funding

Consequences and Control of Randomness in Timing of Intracellular EventsR01GM124446 · NIGMS · UNIVERSITY OF DELAWARE · PI SINGH, ABHYUDAI · 2017 to 2020
$914k
Stochastic hybrid systems approach to uncovering cell-size control mechanisms R01GM126557 · NIGMS · UNIVERSITY OF DELAWARE · PI SINGH, ABHYUDAI · 2017 to 2019
$675k
NIGMS NIH HHS R01 GM124446NIGMS NIH HHS R01 GM126557
6 · The paper itself

Abstract

Chandipura virus (CHPV), a cytoplasmic RNA virus, has been implicated in several outbreaks of acute encephalitis in India. Despite the relevance of CHPV to human health, how the virus interacts with the host signaling machinery remains obscure. In response to viral infections, mammalian cells activate RelA/NF-κB heterodimers, which induce genes encoding interferon beta (IFN-β) and other immune mediators. Therefore, RelA is generally considered to be an antiviral transcription factor. However, RelA activates a wide spectrum of genes in physiological settings, and there is a paucity of direct genetic evidence substantiating antiviral RelA functions. Using mouse embryonic fibroblasts, we genetically dissected the role of RelA in CHPV pathogenesis. We found that CHPV indeed activated RelA and that RelA deficiency abrogated the expression of IFN-β in response to virus infections. Unexpectedly, infection of

Indexed as

Host-Pathogen Interactions3T3 CellsAnimalsCell LineChlorocebus aethiopsEmbryo, MammalianFibroblastsMiceRhabdoviridae InfectionsTranscription Factor RelAVero CellsVesiculovirusRela protein, mouseTranscription Factor RelAburst sizecell deathcytopathicinterferonNF-κBRelARNA virus

Identifiers

PMID31043529
PMCPMC6600208
OpenAlexW2943789579

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.