• Cong Jin, Mifang Liang, Junyu Ning, Wen Gu, Hong Jiang, Wei Wu, Fushun Zhang, Chuan Li, Quanfu Zhang, Hua Zhu, Ting Chen, Ying Han, Weilun Zhang, Shuo Zhang, Qin Wang, Lina Sun, Qinzhi Liu, Jiandong Li, Tao Wang, Qiang Wei, Shiwen Wang, Ying Deng, Chuan Qin, and Dexin Li.
• Laboratory of Viral Hemorrhagic Fever, National Institute for Viral Disease Control and Prevention, China Center for Disease Control Beijing 102206, China.
• Proc. Natl. Acad. Sci. U.S.A. 2012 Jun 19; 109 (25): 10053-8.

AbstractThe discovery of an emerging viral disease, severe fever with thrombocytopenia syndrome (SFTS), caused by SFTS virus (SFTSV), has prompted the need to understand pathogenesis of SFTSV. We are unique in establishing an infectious model of SFTS in C57/BL6 mice, resulting in hallmark symptoms of thrombocytopenia and leukocytopenia. Viral RNA and histopathological changes were identified in the spleen, liver, and kidney. However, viral replication was only found in the spleen, which suggested the spleen to be the principle target organ of SFTSV. Moreover, the number of macrophages and platelets were largely increased in the spleen, and SFTSV colocalized with platelets in cytoplasm of macrophages in the red pulp of the spleen. In vitro cellular assays further revealed that SFTSV adhered to mouse platelets and facilitated the phagocytosis of platelets by mouse primary macrophages, which in combination with in vivo findings, suggests that SFTSV-induced thrombocytopenia is caused by clearance of circulating virus-bound platelets by splenic macrophages. Thus, this study has elucidated the pathogenic mechanisms of thrombocytopenia in a mouse model resembling human SFTS disease.

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