ArticleJournal of virology2012
Suppression of the interferon and NF-κB responses by severe fever with thrombocytopenia syndrome virus.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 1 of them a synthesis that pooled it.
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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.
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.
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Who cites it
83 citing papers in PubMed, 1 synthesis or guideline pooled it, 133 citations in OpenAlex.
- A meta-analysis of multiple matched copy number and transcriptomics data sets for inferring gene regulatory relationships.PloS one · 2014Pooled it
- Differential innate immune activation by wild-type and NSs-deficient RVFV strains in human blood monocytes.Emerging microbes & infections · 2026Article
- Targeting the lethal weakness of SFTSV: Latest advances in antiviral strategies and immune prevention.iScience · 2026Review
- Immune Cells at the Frontline of SFTSV Infection.Journal of microbiology and biotechnology · 2026Review
- Genetically Diverse Severe Fever with Thrombocytopenia Syndrome Virus Circulates in Shelter and Companion Dogs in South Korea.International journal of molecular sciences · 2026Article
- Research progress on antiviral drugs and vaccines for severe fever with thrombocytopenia syndrome.Frontiers in immunology · 2026Review
- Review
- A viral necrosome mediates direct RIPK3 activation to promote inflammatory necroptosis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Review
- Pathogenesis and virulence of Heartland virus.Virulence · 2024Review
- Interaction between the SFTSV envelope glycoprotein Gn and STING inhibits the formation of the STING-TBK1 complex and suppresses the NF-κB signaling pathway.Journal of virology · 2024Article
- Hsp90 β is critical for the infection of severe fever with thrombocytopenia syndrome virus.Virologica Sinica · 2024Article
- Antiviral immunity of severe fever with thrombocytopenia syndrome: current understanding and implications for clinical treatment.Frontiers in immunology · 2024Review
- Aspartate aminotransferase to platelet ratio correlates with poor prognosis and metabolic alterations inFrontiers in immunology · 2024Article
- Innate immune response against vector-borne bunyavirus infection and viral countermeasures.Frontiers in cellular and infection microbiology · 2024Review
- Dabie bandavirus infection induces macrophagic pyroptosis and this process is attenuated by platelets.PLoS neglected tropical diseases · 2023Article
- Article
- Recent Advances in the Study of the Immune Escape Mechanism of SFTSV and Its Therapeutic Agents.Viruses · 2023Review
- Pseudotyped Virus for Bandavirus.Advances in experimental medicine and biology · 2023Article
- The Railmap of Type I Interferon Induction: Subcellular Network Plan and How Viruses Can Change Tracks.Cells · 2022Review
23 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Severe fever with thrombocytopenia syndrome (SFTS) is an emerging infectious disease characterized by high fever, thrombocytopenia, multiorgan dysfunction, and a high fatality rate between 12 and 30%. It is caused by SFTS virus (SFTSV), a novel Phlebovirus in family Bunyaviridae. Although the viral pathogenesis remains largely unknown, hemopoietic cells appear to be targeted by the virus. In this study we report that human monocytes were susceptible to SFTSV, which replicated efficiently, as shown by an immunofluorescence assay and real-time reverse transcription-PCR. We examined host responses in the infected cells and found that antiviral interferon (IFN) and IFN-inducible proteins were induced upon infection. However, our data also indicated that downregulation of key molecules such as mitochondrial antiviral signaling protein (MAVS) or weakened activation of interferon regulatory factor (IRF) and NF-κB responses may contribute to a restricted innate immunity against the infection. NSs, the nonstructural protein encoded by the S segment, suppressed the beta interferon (IFN-β) and NF-κB promoter activities, although NF-κB activation appears to facilitate SFTSV replication in human monocytes. NSs was found to be associated with TBK1 and may inhibit the activation of downstream IRF and NF-κB signaling through this interaction. Interestingly, we demonstrated that the nucleoprotein (N), also encoded by the S segment, exhibited a suppressive effect on the activation of IFN-β and NF-κB signaling as well. Infected monocytes, mainly intact and free of apoptosis, may likely be implicated in persistent viral infection, spreading the virus to the circulation and causing primary viremia. Our findings provide the first evidence in dissecting the host responses in monocytes and understanding viral pathogenesis in humans infected with a novel deadly Bunyavirus.
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Registered trials
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.