SUCLG2 plays a crucial role in the activity of Nitazoxanide against Japanese encephalitis virus
文献类型: 外文期刊
作者: Wei, Min;Ma, Rumeng;Wang, Xiaoyang;Wang, Chunmei;Wang, Mi;Bai, Han;Ye, Wenchong;Zhou, Wen;Zhang, Keyu
作者机构:
关键词: Succinyl-CoA synthetase GDP forming subunit;beta;Japanese encephalitis virus;Nitazoxanide;Interferon beta
期刊名称: ANTIVIRAL RESEARCH
ISSN: 0166-3542
年卷期: 2025 年 244 卷
页码:
收录情况: SCIE(2025版)
摘要: Japanese encephalitis virus (JEV) is the primary causative agent of viral encephalitis, and Nitazoxanide (NTZ) has been shown to exhibit potent antiviral activity against JEV both in vitro and in vivo. Previous studies have demonstrated that NTZ modulates the expression of succinyl-CoA synthetase GDP forming subunit beta (SUCLG2), a GTP-specific succinyl-CoA synthetase, in JEV-infected cells. However, the functional role and underlying mechanism of SUCLG2 in NTZ-mediated antiviral effects against JEV remain poorly understood. In this study, we found that SiRNA-mediated knockdown of SUCLG2 significantly enhanced JEV proliferation in BHK-21 cells, whereas overexpression of SUCLG2 markedly suppressed viral replication. Moreover, SUCLG2 overexpression attenuated ROS production induced by JEV infection and promoted ATP recovery. Furthermore, SUCLG2 activated innate immunity by enhancing IFN-beta expression. Additionally, our findings indicate that SUCLG2 exhibits relatively weak direct binding affinity with NTZ. In conclusion, our results demonstrate that SUCLG2 plays a critical role in mediating the antiviral activity of NTZ against JEV, providing novel insights into the molecular mechanisms underlying NTZ's antiviral efficacy.
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