| Title | Correlation between thrombocytopenia and host response in severe fever with thrombocytopenia syndrome |
| Authors | Li, Xiao-Kun Dai, Ke Yang, Zhen-Dong Yuan, Chun Cui, Ning Zhang, Shao-Fei Hu, Yuan-Yuan Wang, Zhi-Bo Miao, Dong Zhang, Pan-He Li, Hao Zhang, Xiao-Ai Huang, Yan-Qin Chen, Wei-Wei Zhang, Jiu-Song Lu, Qing-Bin Liu, Wei |
| Affiliation | Beijing Inst Microbiol & Epidemiol, State Key Lab Pathogen & Biosecur, Beijing, Peoples R China 990 Hosp Chinese Peoples Liberat Army Joint Logis, Shihe Dist, Xinyang, Peoples R China Shangcheng Ctr Dis Control & Prevent, Xinyang, Shangcheng Coun, Peoples R China Chinese Peoples Liberat Army Gen Hosp, Med Ctr 5, Treatment & Res Ctr Infect Dis, Beijing, Peoples R China Peking Univ, Dept Lab Sci & Technol, Sch Publ Hlth, Beijing, Peoples R China Key Lab Vector Borne & Nat Focus Infect Dis, Beijing, Peoples R China |
| Keywords | PLATELET ACTIVATION INJURY DENGUE CHINA |
| Issue Date | Oct-2020 |
| Publisher | PLOS NEGLECTED TROPICAL DISEASES |
| Abstract | Author summary Thrombocytopenia in SFTSV is a multifactor-process involving a combination of platelet size or morphology alterations, fibrinolysis activation and coagulation abnormalities, increased inflammatory response and endothelial injury. Platelet supplementation alone shows minor role in improving disease, therefore new therapeutic intervention to regulate host response should be proposed. 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. |
| URI | http://hdl.handle.net/20.500.11897/601355 |
| ISSN | 1935-2735 |
| DOI | 10.1371/journal.pntd.0008801 |
| Indexed | SCI(E) |
| Appears in Collections: | 公共卫生学院 |
