Evidence map›Paper›PMID 34413339›Full record

ArticleScientific reports2021

SARS-CoV-2 infection initiates interleukin-17-enriched transcriptional response in different cells from multiple organs.

Md Zobaer Hasan, Syful Islam, Kenichi Matsumoto, Taro Kawai

Open access · goldAbstract readComparative Study
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.7field-weighted citation impact, top 5% 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

42 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. IFN-γ, IL-17, IL-22American journal of clinical and experimental immunology · 2024
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  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

4 authors at 1 institution in 1 country.

Md Zobaer HasanLaboratory of Molecular Immunobiology, Division of Biological Science, Graduate School of Science and Technology, Nara Institute of Science and Technology (NAIST), Nara, 630-0192, Japan. hasan@rohto.co.jp.
Syful IslamLaboratory of Software Engineering, Division of Information Science, Graduate School of Science and Technology, Nara Institute of Science and Technology (NAIST), Nara, 630-0192, Japan.
Kenichi MatsumotoLaboratory of Software Engineering, Division of Information Science, Graduate School of Science and Technology, Nara Institute of Science and Technology (NAIST), Nara, 630-0192, Japan.
Taro KawaiLaboratory of Molecular Immunobiology, Division of Biological Science, Graduate School of Science and Technology, Nara Institute of Science and Technology (NAIST), Nara, 630-0192, Japan. tarokawai@bs.naist.jp.
Nara Institute of Science and Technology · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has emerged as a pandemic. Paucity of information concerning the virus and therapeutic interventions have made SARS-CoV-2 infection a genuine threat to global public health. Therefore, there is a growing need for understanding the molecular mechanism of SARS-CoV-2 infection at cellular level. To address this, we undertook a systems biology approach by analyzing publicly available RNA-seq datasets of SARS-CoV-2 infection of different cells and compared with other lung pathogenic infections. Our study identified several key genes and pathways uniquely associated with SARS-CoV-2 infection. Genes such as interleukin (IL)-6, CXCL8, CCL20, CXCL1 and CXCL3 were upregulated, which in particular regulate the cytokine storm and IL-17 signaling pathway. Of note, SARS-CoV-2 infection strongly activated IL-17 signaling pathway compared with other respiratory viruses. Additionally, this transcriptomic signature was also analyzed to predict potential drug repurposing and small molecule inhibitors. In conclusion, our comprehensive data analysis identifies key molecular pathways to reveal underlying pathological etiology and potential therapeutic targets in SARS-CoV-2 infection.

Indexed as

Antiviral AgentsChemokine CCL20Chemokine CXCL1Chemokines, CXCCOVID-19COVID-19 Drug TreatmentDrug RepositioningHumansInterleukin-17Interleukin-6Interleukin-8Organ SpecificitySARS-CoV-2Signal TransductionSystems BiologyTranscriptomeAntiviral AgentsChemokine CCL20Chemokine CXCL1Chemokines, CXCCXCL3 protein, humanInterleukin-17Interleukin-6Interleukin-8

Identifiers

PMID34413339
PMCPMC8376961
OpenAlexW3195184496

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.