| Literature DB >> 31444469 |
Hao Li1, Lei-Ke Zhang2,3,4, Shu-Fen Li2, Shao-Fei Zhang1, Wei-Wei Wan2, Yu-Lan Zhang2, Qi-Lin Xin2, Ke Dai1, Yuan-Yuan Hu1, Zhi-Bo Wang1, Xiang-Tao Zhu2,3, Yu-Jie Fang2,3, Ning Cui5, Pan-He Zhang1, Chun Yuan5, Qing-Bin Lu6, Jie-Ying Bai7, Fei Deng2,3,4, Geng-Fu Xiao2,3,4, Wei Liu8, Ke Peng9,10,11.
Abstract
Severe fever with thrombocytopenia syndrome (SFTS), an emerging tick-borne infectious disease caused by a novel phlebovirus (SFTS virus, SFTSV), was listed among the top 10 priority infectious diseases by the World Health Organization due to its high fatality of 12%-50% and possibility of pandemic transmission. Currently, effective anti-SFTSV intervention remains unavailable. Here, by screening a library of FDA-approved drugs, we found that benidipine hydrochloride, a calcium channel blocker (CCB), inhibited SFTSV replication in vitro. Benidipine hydrochloride was revealed to inhibit virus infection through impairing virus internalization and genome replication. Further experiments showed that a broad panel of CCBs, including nifedipine, inhibited SFTSV infection. The anti-SFTSV effect of these two CCBs was further analyzed in a humanized mouse model in which CCB treatment resulted in reduced viral load and decreased fatality rate. Importantly, by performing a retrospective clinical investigation on a large cohort of 2087 SFTS patients, we revealed that nifedipine administration enhanced virus clearance, improved clinical recovery, and remarkably reduced the case fatality rate by >5-fold. These findings are highly valuable for developing potential host-oriented therapeutics for SFTS and other lethal acute viral infections known to be inhibited by CCBs in vitro.Entities:
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Year: 2019 PMID: 31444469 PMCID: PMC6796935 DOI: 10.1038/s41422-019-0214-z
Source DB: PubMed Journal: Cell Res ISSN: 1001-0602 Impact factor: 25.617