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A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time
Published on: February 14, 2017
SFTSV infection drives platelet-associated fibrinogen accumulation and platelet-mediated coagulopathy
Chenhui Lin1,2, Ling Xu3, Chaoxiong Yue1
1State Key Laboratory of Virology and Biosafety and National Virus Resource Center, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, Hubei, China.
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 × 109/L vs 50-150 × 109/L). Platelet-associated SFTS virus (SFTSV) nucleoprotein, activation markers (CD62P and activated GPIIb/IIIa), and fibrinogen levels were measured by flow cytometry and Western blot. In vitro infection assays using human and mouse platelets, including UV-inactivated virus controls, were performed to establish causality and assess platelet aggregation and clot turbidity.
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 × 109/L) had higher platelet-associated fibrinogen levels and more pronounced coagulopathy. Platelet fibrinogen levels correlated positively with activation markers and viral load. In vitro, live but not UV-inactivated SFTSV directly induced platelet activation, fibrinogen accumulation, and enhanced aggregation and clot formation in human and mouse platelets. Immunofluorescence revealed that fibrinogen accumulated in association with platelets, with a distribution distinct from that of von Willebrand factor.
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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