Beclin1 Binds to Enterovirus 71 3D Protein to Promote the Virus Replication

Viruses

Pin Wang¹  Zhen Luo¹  Qi Xiang²  Ge Yang²  Mengying Qin²  Jianguo Wu²  Hua Yang²  Siyu Huang²  Kailang Wu² 

[1] Guangdong Provincial Key Laboratory of Virology, Institute of Medical Microbiology, Jinan University, Guangzhou 510632, China;State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, China;

关键词: enterovirus 71;    EV71;    EV71 non-structural protein 3D;    Beclin1;    autophagy;   

DOI  :  10.3390/v12070756

来源: DOAJ

【 摘 要 】

Enterovirus 71 (EV71) is the main pathogen causing hand-foot-mouth disease (HFMD) in infants and children, which can also lead to severe neurological diseases and even death. Therefore, understanding the replication mechanism of EV71 is of great significance for the prevention and control of EV71-induced diseases. Beclin1 (BECN1, a mammalian homologue of ATG6 in yeast) is an important core protein for the initiation and the normal process of autophagy in cells. In addition to its involvement in autophagy, Beclin1 has also been reported to play an important role in cancer and innate immune signaling pathways. However, the role of Beclin1 in EV71 replication remains elusive. Here, we primarily found that Beclin1 facilitates EV71 replication in human rhabdomyosarcoma (RD) cells and the autophagy was actually induced, but Beclin1 was not significantly affected at either mRNA level or protein level during early EV71 infection. Further studies discovered that Beclin1 could interacts with EV71 non-structural protein 3D mainly through its evolutionary conserved domain (ECD) and coiled-coiled domain (CCD), thus promoting the replication of EV71 in human rhabdomyosarcoma (RD) cells and human astroglioma (U251) cells. Collectively, we reveal a novel regulatory mechanism associated with Beclin1 to promote EV71 replication, thus providing a potential therapeutic target for the prevention and control of EV71-associated diseases.

【 授权许可】

Unknown