Fang Yaohui, Shen Shu, Zhang Jingyuan, Xu Ling, Wang Tong, Fan Lei, Zhu Qiong, Xiao Jian, Wu Xiaoli, Jin Jiayin, Wu Qiaoli, Zhang Yanfang, Tang Shuang, Zheng Xin, Deng Fei
Key Laboratory of Virology and Biosafety and National Virus Resource Center, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, China.
University of Chinese Academy of Sciences, Beijing, People's Republic of China.
J Infect Dis. 2025 Feb 4;231(1):e183-e194. doi: 10.1093/infdis/jiae355.
Thrombocytopenia is the major clinical feature of severe fever with thrombocytopenia syndrome (SFTS), but the mechanism by which it occurs remains unclear.
RNA transcriptome analyses were performed on platelets purified from patients with SFTS and mice infected with SFTS virus (SFTSV). The functions of differentially expressed genes (DEGs) in the platelets were characterized. Enzyme-linked immunosorbent assay, flow cytometry, and quantitative reverse-transcription polymerase chain reaction were used to measure the levels of platelet activation, SFTSV infection in platelets, formation of neutrophil extracellular traps, transcription of DEGs, and the percentage of platelets undergoing cell death.
Enhanced neutrophil activation and interferon signaling involved in the viral life cycle were common platelet responses in SFTS, which may consume increasing numbers of platelets. Other functional changes may be associated with different outcomes of SFTS. SFTSV infection led to platelet destruction by pyroptosis, apoptosis, necroptosis, and autophagy. Platelets in SFTSV-infected mice mainly play a role in adaptive immunity, and platelet death was not as severe as in humans.
The altered functions of platelets, including mediating leukocyte activation and undergoing cell death, contribute to thrombocytopenia in patients with SFTS. The different mechanisms of thrombocytopenia in mice suggest that platelet functions should be considered in experimental animal models.
血小板减少是发热伴血小板减少综合征（SFTS）的主要临床特征，但其发生机制尚不清楚。
对从SFTS患者和感染SFTS病毒（SFTSV）的小鼠中纯化的血小板进行RNA转录组分析。对血小板中差异表达基因（DEG）的功能进行了表征。采用酶联免疫吸附测定、流式细胞术和定量逆转录聚合酶链反应来测量血小板活化水平、血小板中的SFTSV感染、中性粒细胞胞外陷阱的形成、DEG的转录以及发生细胞死亡的血小板百分比。
参与病毒生命周期的中性粒细胞活化增强和干扰素信号传导是SFTS中常见的血小板反应，这可能消耗越来越多的血小板。其他功能变化可能与SFTS的不同结局相关。SFTSV感染导致血小板通过焦亡、凋亡、坏死性凋亡和自噬而被破坏。感染SFTSV的小鼠中的血小板主要在适应性免疫中起作用，并且血小板死亡不如人类严重。
血小板功能的改变，包括介导白细胞活化和发生细胞死亡，导致SFTS患者出现血小板减少。小鼠中血小板减少的不同机制表明，在实验动物模型中应考虑血小板功能。
