ArticleVirus research2023
Screening core genes and signaling pathways after SFTSV infection by integrated transcriptome profiling analysis.
Article in Virus research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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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
6 citing papers in PubMed, 5 citations in OpenAlex.
- RNAi Regulator C3PO Promotes Arbovirus Infection in Insect Vectors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Multidimensional mechanisms of SFTSV-host interactions: viral protein functions, mFrontiers in cellular and infection microbiology · 2026Review
- Multi-omics analysis of SFTS virus infection in Rhipicephalus microplus cells reveals antiviral tick factors.Nature communications · 2025Article
- Alterations in the salivary gland microbiota ofZoological research · 2025Article
- Haemaphysalis longicornis subolesin controls the infection and transmission of severe fever with thrombocytopenia syndrome virus.NPJ vaccines · 2025Article
- Transcriptome Profiles Characteristics of the Peripheral Immune in Patients with Severe Fever with Thrombocytopenia Syndrome.Journal of inflammation research · 2024Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A newly discovered tick-borne virus called the severe fever with thrombocytopenia syndrome virus (SFTSV) can cause the severe fever with thrombocytopenia syndrome (SFTS). The mortality and incidence rate of SFTS patients remain extremely high due to the fast global dissemination of its arthropod vectors, and the mechanism of viral pathogenesis remains largely unknown. In this study, high-throughput RNA sequencing (RNA-Seq) was used to sequence HEK 293 cells treated with SFTSV at four time points. 115, 191, 259, and 660 differentially expressed genes (DEGs) were identified at 6, 12, 24, and 48 h post-infection, respectively. We found that SFTSV infection induced the expression of genes responsible for numerous cytokine-related pathways, including TNF, CXCL1, CXCL2, CXCL3, CXCL8, CXCL10, and CCL20. With the extension of infection time, the expression of most genes involved in these pathways increased significantly, indicating the host's inflammatory response to SFTSV. Moreover, the expression levels of GNA13, ARHGEF12, RHOA, ROCK1, and MYL12A, elements of the platelet activation signaling pathway, were downregulated during SFTSV infection, suggesting that the SFTSV infection may cause thrombocytopenia by inhibiting platelet activation. Our results contribute to further understanding the interaction between SFTSV and the host.
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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 Socratic graph.