Title Caspase-3 inhibitor inhibits enterovirus D68 production
Author Wenbo Huo1,2, Jinghua Yu1, Chunyu Liu3, Ting Wu4, Yue Wang5, Xiangling Meng2, Fengmei Song2, Shuxia Zhang2, Ying Su2, Yumeng Liu2, Jinming Liu2, Xiaoyan Yu2, and Shucheng Hua6
Address 1Institute of Virology and AIDS Research, The First Hospital of Jilin University, Jilin University, Changchun 130000, P. R. China, 2Department of Experimental Pharmacology and Toxicology, School of Pharmaceutical Science, Jilin University, Changhun 130000, P. R. China, 3Acupuncture Department, The Affiliated Hospital of Changchun University of Chinese Medicine, Changchun 130000, P. R. China, 4Neonatal Intensive Care Unit, The First Hospital of Jilin University, Jilin University, Changchun 130000, P. R. China, 5Department of Chemistry of Traditional Chinese Medicine, Changchun University of Chinese Medicine, Changchun 130000, P. R. China, 6Department of Internal Medicine, The First Hospital of Jilin University, Jilin University, Changchun 130000, P. R. China
Bibliography Journal of Microbiology, 58(9),812–820, 2020,
DOI 10.1007/s12275-020-0241-y
Key Words EVD68, caspase-3, apoptosis, viral production, host-pathogen interaction
Abstract Enterovirus D68 (EVD68) is an emerging pathogen that recently caused a large worldwide outbreak of severe respiratory disease in children. However, the relationship between EVD68 and host cells remains unclear. Caspases are involved in cell death, immune response, and even viral production. We found that caspase-3 was activated during EVD68 replication to induce apoptosis. Caspase-3 inhibitor (Z-DEVDFMK) inhibited viral production, protected host cells from the cytopathic effects of EVD68 infection, and prevented EVD68 from regulating the host cell cycle at G0/G1. Meanwhile, caspase-3 activator (PAC-1) increased EVD68 production. EVD68 infection therefore activates caspase-3 for virus production. This knowledge provides a potential direction for the prevention and treatment of disease related to EVD68.