Evidence map›Paper›PMID 28609011›Full record

ArticleJournal of cellular and molecular medicine2017

The highly pathogenic H5N1 influenza A virus down-regulated several cellular MicroRNAs which target viral genome.

Rong Wang, Ying-Ying Zhang, Jian-Sheng Lu, Bing-Hui Xia, Zhi-Xin Yang, Xu-Dong Zhu, Xiao-Wei Zhou, Pei-Tang Huang

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Cross Talk between MicroRNAs and Dengue Virus.The American journal of tropical medicine and hygiene · 2024
    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

8 authors at 2 institutions in 1 country.

Rong WangLaboratory of Protein Engineering, Beijing Institute of Biotechnology, Beijing, China.ORCID http://orcid.org/0000-0003-1515-2683
Ying-Ying ZhangLaboratory of Protein Engineering, Beijing Institute of Biotechnology, Beijing, China.
Jian-Sheng LuLaboratory of Protein Engineering, Beijing Institute of Biotechnology, Beijing, China.
Bing-Hui XiaLaboratory of Protein Engineering, Beijing Institute of Biotechnology, Beijing, China.
Zhi-Xin YangLaboratory of Protein Engineering, Beijing Institute of Biotechnology, Beijing, China.
Xu-Dong ZhuLaboratory of Protein Engineering, Beijing Institute of Biotechnology, Beijing, China.
Xiao-Wei ZhouLaboratory of Protein Engineering, Beijing Institute of Biotechnology, Beijing, China.
Pei-Tang HuangLaboratory of Protein Engineering, Beijing Institute of Biotechnology, Beijing, China.
Beijing Proteome Research Center · CNAir Force General Hospital PLA · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Higher and prolonged viral replication is critical for the increased pathogenesis of the highly pathogenic avian influenza (HPAI) subtype of H5N1 influenza A virus (IAV) over the lowly pathogenic H1N1 IAV strain. Recent studies highlighted the considerable roles of cellular miRNAs in host defence against viral infection. In this report, using a 3'UTR reporter system, we identified several putative miRNA target sites buried in the H5N1 virus genome. We found two miRNAs, miR-584-5p and miR-1249, that matched with the PB2 binding sequence. Moreover, we showed that these miRNAs dramatically down-regulated PB2 expression, and inhibited replication of H5N1 and H1N1 IAVs in A549 cells. Intriguingly, these miRNAs expression was differently regulated in A549 cells infected with the H5N1 and H1N1 viruses. Furthermore, transfection of miR-1249 inhibitor enhanced the PB2 expression and promoted the replication of H5N1 and H1N1 IAVs. These results suggest that H5N1 virus may have evolved a mechanism to escape host-mediated inhibition of viral replication through down-regulation of cellular miRNAs, which target its viral genome.

Indexed as

Genome, ViralHost-Pathogen Interactions3' Untranslated RegionsA549 CellsAnimalsAntagomirsBase SequenceBinding SitesDogsGene Expression RegulationGenes, ReporterHEK293 CellsHumansInfluenza A Virus, H1N1 SubtypeInfluenza A Virus, H5N1 SubtypeLuciferases3' Untranslated RegionsAntagomirsLuciferasesMicroRNAsMIRN584 microRNA, humanPB2 protein, Influenzavirus ARNA-Dependent RNA PolymeraseViral ProteinsH1N1H5N1 HPAIhost defenceMicroRNAsvirus replication

Identifiers

PMID28609011
PMCPMC5661113
OpenAlexW2626114280

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.