Evidence map›Paper›PMID 28234991›Full record

ArticlePloS one2017

Severe fever with thrombocytopenia syndrome virus inhibits exogenous Type I IFN signaling pathway through its NSs invitro.

Xu Chen, Haiyan Ye, Shilin Li, Baihai Jiao, Jianqin Wu, Peibin Zeng, Limin Chen

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

35 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Immune Cells at the Frontline of SFTSV Infection.Journal of microbiology and biotechnology · 2026
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  12. Emerging Tick-BorneMicroorganisms · 2023
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  16. Review
  17. The development of COVID-19 treatment.Frontiers in immunology · 2023
    Review
  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

7 authors at 3 institutions in 2 countries.

Xu ChenInstitute of Blood Transfusion, Chinese Academic of Medical Sciences and Peking Union Medical College, Chengdu, China.
Haiyan YeInstitute of Blood Transfusion, Chinese Academic of Medical Sciences and Peking Union Medical College, Chengdu, China.
Shilin LiInstitute of Blood Transfusion, Chinese Academic of Medical Sciences and Peking Union Medical College, Chengdu, China.
Baihai JiaoInstitute of Blood Transfusion, Chinese Academic of Medical Sciences and Peking Union Medical College, Chengdu, China.
Jianqin WuInstitute of Blood Transfusion, Chinese Academic of Medical Sciences and Peking Union Medical College, Chengdu, China.
Peibin ZengWest China School of Public Health, Sichuan University, Chengdu, Sichuan, China.
Limin ChenInstitute of Blood Transfusion, Chinese Academic of Medical Sciences and Peking Union Medical College, Chengdu, China.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNSichuan University · CNUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Severe fever with thrombocytopenia syndrome (SFTS) is an emerging infectious disease caused by a novel bunyavirus (SFTS virus, SFTSV). At present there is still no specific antiviral treatment for SFTSV; To understand which cells support SFTSV life cycle and whether SFTSV infection activates host innate immunity, four different cell lines (Vero, Hela, Huh7.5.1, and Huh7.0) were infected with SFTSV. Intracellular/extracellular viral RNA and expression of IFNα, and IFNß were detected by real-time RT- PCR following infection. To confirm the role of non-structural protein (NSs) of SFTSV in exogenous IFNα-induced Jak/STAT signaling, p-STAT1 (Western Blot), ISRE activity (Luciferase assay) and ISG expression (real-time PCR) were examined following IFNα stimulation in the presence or absence of over-expression of NSs in Hela cells. Our study showed that all the four cell lines supported SFTSV life cycle and SFTSV activated host innate immunity to produce type I IFNs in Hela cells but not in Huh7.0, Huh7.5.1 or Vero cells. NSs inhibited exogenous IFNα-induced Jak/STAT signaling as shown by decreased p-STAT1 level, suppressed ISRE activity and down-regulated ISG expression. Suppression of the exogenous Type I IFN-induced Jak/STAT signaling by NSs might be one of the mechanisms of SFTSV to evade host immune surveillance.

Indexed as

AnimalsBunyaviridae InfectionsChlorocebus aethiopsHeLa CellsHost-Parasite InteractionsHumansImmunity, InnateInterferon Type IPhlebovirusSignal TransductionVero CellsViral Nonstructural ProteinsInterferon Type IViral Nonstructural Proteins

Identifiers

PMID28234991
PMCPMC5325526
OpenAlexW2590317312

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.