Evidence map›Paper›PMID 39273091›Full record

ArticleInternational journal of molecular sciences2024

Rabies Virus Regulates Inflammatory Response in BV-2 Cells through Activation of Myd88 and NF-κB Signaling Pathways via TLR7.

Yuan Xie, Yinglin Chi, Xiaoyan Tao, Pengcheng Yu, Qian Liu, Minghui Zhang, Nuo Yang, Shuqing Liu, Wuyang Zhu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
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.

Yuan XieKey Laboratory of Medical Virology, Ministry of Health, National Institute for Viral Disease Control and Prevention, NHC Key Laboratory of Biosafety, Chinese Center for Disease Control and Prevention, Beijing 102206, China.
Yinglin ChiKey Laboratory of Medical Virology, Ministry of Health, National Institute for Viral Disease Control and Prevention, NHC Key Laboratory of Biosafety, Chinese Center for Disease Control and Prevention, Beijing 102206, China.
Xiaoyan TaoKey Laboratory of Medical Virology, Ministry of Health, National Institute for Viral Disease Control and Prevention, NHC Key Laboratory of Biosafety, Chinese Center for Disease Control and Prevention, Beijing 102206, China.
Pengcheng YuKey Laboratory of Medical Virology, Ministry of Health, National Institute for Viral Disease Control and Prevention, NHC Key Laboratory of Biosafety, Chinese Center for Disease Control and Prevention, Beijing 102206, China.
Qian LiuKey Laboratory of Medical Virology, Ministry of Health, National Institute for Viral Disease Control and Prevention, NHC Key Laboratory of Biosafety, Chinese Center for Disease Control and Prevention, Beijing 102206, China.
Minghui ZhangKey Laboratory of Medical Virology, Ministry of Health, National Institute for Viral Disease Control and Prevention, NHC Key Laboratory of Biosafety, Chinese Center for Disease Control and Prevention, Beijing 102206, China.
Nuo YangKey Laboratory of Medical Virology, Ministry of Health, National Institute for Viral Disease Control and Prevention, NHC Key Laboratory of Biosafety, Chinese Center for Disease Control and Prevention, Beijing 102206, China.
Shuqing LiuKey Laboratory of Medical Virology, Ministry of Health, National Institute for Viral Disease Control and Prevention, NHC Key Laboratory of Biosafety, Chinese Center for Disease Control and Prevention, Beijing 102206, China.ORCID 0000-0002-9412-3436
Wuyang ZhuKey Laboratory of Medical Virology, Ministry of Health, National Institute for Viral Disease Control and Prevention, NHC Key Laboratory of Biosafety, Chinese Center for Disease Control and Prevention, Beijing 102206, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rabies is a fatal neurological infectious disease caused by rabies virus (RABV), which invades the central nervous system (CNS). RABV with varying virulence regulates chemokine expression, and the mechanisms of signaling pathway activation remains to be elucidated. The relationship between Toll-like receptors (TLRs) and immune response induced by RABV has not been fully clarified. Here, we investigated the role of TLR7 in the immune response induced by RABV, and one-way analysis of variance (ANOVA) was employed to evaluate the data. We found that different RABV strains (SC16, HN10, CVS-11) significantly increased CCL2, CXCL10 and IL-6 production. Blocking assays indicated that the TLR7 inhibitor reduced the expression of CCL2, CXCL10 and IL-6 (

Indexed as

Myeloid Differentiation Factor 88NF-kappa BRabies virusSignal TransductionToll-Like Receptor 7AnimalsCell LineChemokine CCL2Chemokine CXCL10InflammationInterleukin-6Membrane GlycoproteinsMiceRabiesTranscription Factor RelAChemokine CCL2Chemokine CXCL10Interleukin-6Membrane GlycoproteinsMyd88 protein, mouseMyeloid Differentiation Factor 88NF-kappa BRela protein, mouseTlr7 protein, mouseToll-Like Receptor 7Transcription Factor RelAMyd88NF-κB pathwayrabies virusTLR7

Identifiers

PMID39273091
PMCPMC11395267

What OpenQuestion holds

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Registered trials

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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.