| Literature DB >> 32870487 |
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, Shucheng Hua6.
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-DEVD-FMK) 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.Entities:
Keywords: EVD68; apoptosis; caspase-3; host-pathogen interaction; viral production
Mesh:
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Year: 2020 PMID: 32870487 PMCID: PMC7459088 DOI: 10.1007/s12275-020-0241-y
Source DB: PubMed Journal: J Microbiol ISSN: 1225-8873 Impact factor: 3.422