ArticleResearch and practice in thrombosis and haemostasis2026
SFTSV infection drives platelet-associated fibrinogen accumulation and platelet-mediated coagulopathy.
Article in Research and practice in thrombosis and haemostasis, 2026. 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
Background: Severe fever with thrombocytopenia syndrome (SFTS) is an emerging viral hemorrhagic fever characterized by high mortality, thrombocytopenia, and coagulation abnormalities. Unlike other inflammatory conditions where plasma fibrinogen rises, patients with SFTS exhibit normal fibrinogen levels despite evidence of consumptive coagulopathy and hepatocyte injury. Objectives: The aim of this study was to investigate whether platelets contribute to fibrinogen dysregulation and coagulopathy in SFTS. Methods: We enrolled 102 patients with SFTS stratified by clinical symptoms (mild vs severe) and by platelet count (<50 × 10 Results: Patients with SFTS exhibited significant platelet activation and elevated platelet-associated fibrinogen levels despite normal plasma levels. Patients with severe thrombocytopenia (platelet count <50 × 10 Conclusion: SFTSV infection drives platelet activation and fibrinogen association, potentially leading to enhanced clot formation and contributing to thrombocytopenia. This platelet-centric pathway provides a mechanistic explanation for the distinct coagulopathy of SFTS and identifies platelet fibrinogen as a potential therapeutic target.
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