Enterovirus 71 Induces INF2 Cleavage via Activated Caspase-2 in Infected RD Cells

Frontiers in Microbiology

卷:12

Zhendong Zhao¹  Chongyang Zhang¹  Bei Wang²  Qing Tang³  He Huang³  Congci Yu³  Yue Zhu³ 

[1] Peking Union Medical College, Beijing, China;

[2] Clinical Immunology Center, Chinese Academy of Medical Sciences &

[3] National Health Commission (NHC) Key Laboratory of Systems Biology of Pathogens, Institute of Pathogen Biology, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China;

关键词: EV71;    INF2;    caspase-2;    mitochondrial;    viral replication;   

DOI  :  10.3389/fmicb.2021.684953

来源: DOAJ

【 摘 要 】

Enterovirus 71 (EV71) is the major causative pathogen of hand, foot, and mouth disease. The lack of understanding of the virus’s pathogenesis hinders the development of anti-virus drugs and the control of EV71 infection. Our previous studies have demonstrated that both mitochondria and endoplasmic reticulum (ER) were altered significantly in EV71 infected cells, but the mechanism is still unclear. In this study, we investigated the effects of EV71 infection on the expression of INF2, a key regulator factor in ER-Mitochondria communication and mitochondrial fission. We found that INF2 was cleaved in EV71 infected RD cells. The INF2 cleavage occurred at Aspartic 1,051 of INF2 and is mediated by activated caspases, predominantly by activated caspase-2. The subcellular localization of INF2 and caspase-2 was significantly altered in infected cells. We speculate that caspase-2-mediated INF2 cleavage is involved in forming viral replication organelles (ROs) and is a positive feedback regulatory mechanism of mitochondrial disorders caused by EV71 infection.

【 授权许可】

Unknown