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Caspase-3 inhibitor inhibits enterovirus D68 production.
Journal of Microbiology ( IF 3 ) Pub Date : 2020-09-01 , DOI: 10.1007/s12275-020-0241-y
Wenbo Huo 1, 2 , Jinghua Yu 1 , Chunyu Liu 3 , Ting Wu 4 , Yue Wang 5 , Xiangling Meng 2 , Fengmei Song 2 , Shuxia Zhang 2 , Ying Su 2 , Yumeng Liu 2 , Jinming Liu 2 , Xiaoyan Yu 2 , Shucheng Hua 6
Affiliation  

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.

中文翻译:

Caspase-3抑制剂抑制肠道病毒D68的产生。

肠道病毒D68(EVD68)是一种新兴病原体,最近在世界范围内引起了儿童严重呼吸道疾病的大规模爆发。但是,EVD68与宿主细胞之间的关系仍不清楚。半胱天冬酶参与细胞死亡,免疫反应,甚至病毒产生。我们发现,caspase-3在EVD68复制过程中被激活以诱导凋亡。Caspase-3抑制剂(Z-DEVD-FMK)抑制病毒产生,保护宿主细胞免受EVD68感染的细胞病变作用,并阻止EVD68调节宿主细胞在G0 / G1的周期。同时,caspase-3激活剂(PAC-1)增加了EVD68的产量。因此,EVD68感染激活caspase-3产生病毒。这些知识为预防和治疗与EVD68相关的疾病提供了潜在的方向。
更新日期:2020-09-01
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