ArticleMicrobiology spectrum2025
Blood transcriptomic profiling reveals gene expression alterations in patients with SFTS-associated encephalitis.
Article in Microbiology spectrum, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Severe fever with thrombocytopenia syndrome (SFTS), a life-threatening tick-borne zoonosis caused by severe fever with thrombocytopenia syndrome virus (SFTSV), frequently leads to fatal encephalitis characterized by consciousness disorders and seizures. The molecular mechanisms governing SFTSV neuroinvasion and host-driven neural injury remain largely elusive. To explore the mechanisms of SFTS-induced brain damage, we analyzed clinical laboratory parameters and conducted transcriptomic analyses of peripheral blood mononuclear cells from five SFTS patients with encephalitis and five non-encephalitis patients admitted to Nanjing Drum Tower Hospital during the same period. Our findings indicate that central nervous system manifestations in SFTSV infection are associated with altered expression of immune-related genes. Specifically, we identified six differentially expressed immune genes-MET, KIT, IL1R2, MAFF, CD69, and CEBPD-between the encephalitis and non-encephalitis groups. This study provides novel insights into the pathogenesis of SFTS-associated encephalitis, and further investigation into the host immune response post-SFTSV infection may aid in mitigating disease progression and improving clinical outcomes. IMPORTANCE Severe fever with thrombocytopenia syndrome (SFTS) is a life-threatening disease that can lead to encephalitis-a serious brain inflammation with high mortality. However, the causes of this brain damage remain largely unknown. In this study, we used advanced gene sequencing techniques to analyze blood samples from SFTS patients with and without encephalitis. Our results revealed key changes in immune-related genes, uncovering possible biological pathways involved in brain injury caused by the virus. These findings shed new light on how the immune system may contribute to neurological complications in SFTS and highlight specific genes that could serve as future targets for diagnosis or treatment. This research enhances our understanding of SFTS-related encephalitis and provides a valuable foundation for developing therapies to improve patient outcomes.
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