State Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, P. R. China.
The 990 Hospital of Chinese People's Liberation Army Joint Logistic Support Force, Shihe District, Xinyang, P. R. China.
PLoS Negl Trop Dis. 2020 Oct 29;14(10):e0008801. doi: 10.1371/journal.pntd.0008801. eCollection 2020 Oct.
Severe Fever with Thrombocytopenia Syndrome (SFTS) is an emerging infectious disease caused by a novel bunyavirus, SFTS virus (SFTSV), with fatal outcome developed in approximately 17% of the cases. Thrombocytopenia is a hallmark feature of SFTS, and associated with a higher risk of fatal outcome, however, the pathophysiological involvement of platelet in the clinical outcome of SFTS remained under-investigated. In the current study, by retrospectively analyzing 1538 confirmed SFTS patients, we observed that thrombocytopenia was associated with enhanced activation of the cytokine network and the vascular endothelium, also with a disturbed coagulation response. The platelet phenotypes were also extensively altered in the process of thrombocytopenia development of SFTS patients. More importantly, all these disturbed host responses were related to the severity of thrombocytopenia, thus were considered to play in a synergistic way to influence the disease outcome. Moreover, the clinical effect of platelet transfusion was assessed by comparing two groups of patients with or without receiving this therapy. As a result, we observed no therapy effect in altering frequencies of fatal outcome, clinical bleeding development, or dynamic change of platelet count during the hospitalization. It's suggested that platelet supplementation alone acted a minor role in improving disease outcome, therefore new therapeutic intervention to regulate host response should be proposed. The current results revealed some evidence of interrelationship between platelet count and clinical outcome of SFTS disease from the perspective of activation of the cytokine network, the vascular endothelium, and the coagulation/fibrinolysis system. These evaluations might help to attain a better understanding of the pathogenesis and therapy choice in SFTS.
发热伴血小板减少综合征(SFTS)是一种新发传染病,由一种新型布尼亚病毒SFTS 病毒(SFTSV)引起,约 17%的病例出现致命结局。血小板减少是 SFTS 的一个显著特征,与更高的致命风险相关,但血小板在 SFTS 临床结局中的病理生理作用仍研究不足。在本研究中,通过回顾性分析 1538 例确诊的 SFTS 患者,我们观察到血小板减少与细胞因子网络和血管内皮的过度激活有关,同时也与凝血反应紊乱有关。在 SFTS 患者血小板减少的发展过程中,血小板表型也发生了广泛改变。更重要的是,所有这些受干扰的宿主反应都与血小板减少的严重程度有关,因此被认为是协同作用影响疾病结局。此外,通过比较两组接受或未接受血小板输注治疗的患者,评估了血小板输注的临床效果。结果观察到,在改变死亡率、临床出血发展或住院期间血小板计数的动态变化方面,治疗没有效果。这表明,单独补充血小板在改善疾病结局方面作用较小,因此应提出新的治疗干预措施来调节宿主反应。目前的结果从细胞因子网络、血管内皮和凝血/纤溶系统的激活角度揭示了血小板计数与 SFTS 疾病临床结局之间的一些相互关系证据。这些评估可能有助于更好地理解 SFTS 的发病机制和治疗选择。