ArticleJournal of virology2025
SFTSV utilizes AXL/GAS6 for entry via PI3K-PLC-dependent macropinocytosis activated by AXL-kinase.
Article in Journal of virology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 4 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.
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.
Who cites it
4 citing papers in PubMed.
- Interplay between SFTSV and host innate immunity: Viral evasion mechanisms, pathogenesis, and therapeutic perspectives.iScience · 2026Review
- Exploring SNPs in viral entry-related protein genes and their association with severe fever with thrombocytopenia syndrome virus infection risk.Microbiology spectrum · 2026Article
- Review
- Multidimensional mechanisms of SFTSV-host interactions: viral protein functions, mFrontiers in cellular and infection microbiology · 2026Review
Corrections and comments
- Erratum issued
Authors and funding
10 authors.
Funding
Abstract
Severe fever with thrombocytopenia syndrome (SFTS) is a significant public health concern caused by SFTS virus (SFTSV), a tick-borne RNA virus. Previous studies have identified DC-SIGN and related C-type lectins as receptors of SFTSV infection in specific cell populations. Our genome-wide CRISPR activation screening identified AXL, a receptor tyrosine kinase, as a novel entry receptor for SFTSV. We found that AXL-mediated SFTSV infection utilizes the bridging action of growth arrest-specific protein 6 between AXL and phosphatidylserine on virus particles. This interaction induces autophosphorylation of tyrosine residues in the intracellular domain of AXL, recruiting phosphatidylinositol-3 kinase (PI3K) and phospholipase C (PLC) and establishing a macropinocytotic pathway of SFTSV entry. The AXL-PI3K-PLC-dependent entry pathway was observed in diverse cell types, including human umbilical vein endothelial cells (HUVEC), offering deep insights into the lifecycle of SFTSV and offering AXL as a novel therapeutic target against SFTS.IMPORTANCEUnderstanding the molecular mechanisms of viral entry is critical for developing targeted antiviral therapies since there is no effective vaccine or antiviral drug against severe fever with thrombocytopenia syndrome (SFTS). This study uncovered AXL as a potential entry receptor for SFTS virus (SFTSV) via PI3K/PLC-dependent macropinocytosis pathway distinct from previously reported viral entry mechanism. The inhibition of these cellular enzymes resulted in the suppression of SFTSV infection in the AXL-expressing cell lines and HUVEC. Our research sheds light on the intricate molecular mechanisms underlying these interactions by utilizing mutants of AXL and represents a promising target for the development of innovative therapeutics against SFTS.
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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.