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. |