Evidence map›Paper›PMID 31191546›Full record

ArticleFrontiers in immunology2019

Interferon-γ-Directed Inhibition of a Novel High-Pathogenic Phlebovirus and Viral Antagonism of the Antiviral Signaling by Targeting STAT1.

Yun-Jia Ning, Qiong Mo, Kuan Feng, Yuan-Qin Min, Mingyue Li, Dianhai Hou, Cheng Peng, Xin Zheng, Fei Deng, Zhihong Hu and 1 more

Abstract read
In one paragraph

Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing 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

29 citing papers in PubMed.

  1. Review
  2. Immune Cells at the Frontline of SFTSV Infection.Journal of microbiology and biotechnology · 2026
    Review
  3. Multidimensional mechanisms of SFTSV-host interactions: viral protein functions, mFrontiers in cellular and infection microbiology · 2026
    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

11 authors.

Yun-Jia NingState Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, China.
Qiong MoState Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, China.
Kuan FengState Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, China.
Yuan-Qin MinState Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, China.
Mingyue LiDepartment of Infectious Diseases, Union Hospital, Institute of Infection and Immunology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Dianhai HouState Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, China.
Cheng PengDepartment of Infectious Diseases, Union Hospital, Institute of Infection and Immunology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Xin ZhengDepartment of Infectious Diseases, Union Hospital, Institute of Infection and Immunology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Fei DengState Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, China.
Zhihong HuState Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, China.
Hualin WangState Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Severe fever with thrombocytopenia syndrome (SFTS) is a life-threatening infectious disease caused by a novel phlebovirus, SFTS virus (SFTSV). Currently, there is no vaccine or antiviral available and the viral pathogenesis remains largely unknown. In this study, we demonstrated that SFTSV infection results in substantial production of serum interferon-γ (IFN-γ) in patients and then that IFN-γ in turn exhibits a robust anti-SFTSV activity in cultured cells, indicating the potential role of IFN-γ in anti-SFTSV immune responses. However, the IFN-γ anti-SFTSV efficacy was compromised once viral infection had been established. Consistently, we found that viral nonstructural protein (NSs) expression counteracts IFN-γ signaling. By protein interaction analyses combined with mass spectrometry, we identified the transcription factor of IFN-γ signaling pathway, STAT1, as the cellular target of SFTSV for IFN-γ antagonism. Mechanistically, SFTSV blocks IFN-γ-triggered STAT1 action through (1) NSs-STAT1 interaction-mediated sequestration of STAT1 into viral inclusion bodies and (2) viral infection-induced downregulation of STAT1 protein level. Finally, the efficacy of IFN-γ as an anti-SFTSV drug

Indexed as

AnimalsAntiviral AgentsBunyaviridae InfectionsChlorocebus aethiopsHEK293 CellsHep G2 CellsHost-Pathogen InteractionsHumansInterferon-gammaMice, Inbred ICRPhlebovirusSignal TransductionSTAT1 Transcription FactorVero CellsViral Nonstructural ProteinsAntiviral AgentsInterferon-gammaSTAT1 Transcription FactorViral Nonstructural Proteinsantiviral immunityIFN-γimmune evasioninclusion bodyNSssevere fever with thrombocytopenia syndrome virus (SFTSV)STAT1virus-host interaction

Identifiers

PMID31191546
PMCPMC6546826

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.