. doi: 10.1016/j.virs.2022.11.006
Citation: Jie Fan, Xinqian Lv, Saixia Yang, Shuxian Geng, Jifei Yang, Yaru Zhao, Zhonghui Zhang, Zhijie Liu, Guiquan Guan, Jianxun Luo, Qiaoying Zeng, Hong Yin, Qingli Niu. OGG1 inhibition suppresses African swine fever virus replication .VIROLOGICA SINICA, 2023, 38(1) : 96-107.  http://dx.doi.org/10.1016/j.virs.2022.11.006

OGG1小分子抑制剂对ASFV复制的影响

  • 非洲猪瘟病毒(ASFV)是一种重要的病原体,感染猪后会引起具有高度传染性和致命性的疫病,目前国内尚无有效疫苗和治疗药物可用。8-oxoguanine DNA糖基化酶1(OGG1),是切除氧化碱基损伤8-oxo-7,8-二氢鸟嘌呤(8-oxoG)的重要DNA修复酶,已被证实参与有些病毒感染的发病机制。然而,OGG1-BER (碱基切除修复)在ASFV感染中的作用还未得到证实。本研究旨在验证ASFV感染宿主后胞内活性氧(ROS),8-oxoG和OGG1的变化,并分析OGG1在ASFV感染中的作用。研究发现ASFV感染可引起ROS和8-oxoG的升高和动态变化,并导致OGG1的表达改变。用OGG1的小分子抑制剂TH5487和SU0268处理感染ASFV的猪肺泡巨噬细胞(PAM)后,发现病毒转录水平、翻译水平以及病毒产量明显下降。ASFV的BER通路相关蛋白表达在药物处理后也被抑制。此外,在ASFV感染过程中,OGG1可与病毒MGF360-14L蛋白相互作用并影响干扰素β(IFN-β)的产生。利用TH5487和SU0268小分子化合物或小RNA干扰抑制OGG1后可上调IFN-β的转录,进而影响ASFV的复制。以上结果显示,OGG1在病毒感染中起着至关重要的作用,OGG1抑制剂SU0268和TH5487可作为抗ASFV感染的预防性药物用于进一步研究。

OGG1 inhibition suppresses African swine fever virus replication

  • African swine fever virus (ASFV) is an important pathogen that causes a highly contagious and lethal disease in swine, for which neither a vaccine nor treatment is available. The DNA repair enzyme 8-oxoguanine DNA glycosylase 1 (OGG1), which excises the oxidative base lesion 8-oxo-7,8-dihydroguanine (8-oxoG), has been linked to the pathogenesis of different diseases associated with viral infections. However, the role of OGG1-base excision repair (BER) in ASFV infection has been poorly investigated. Our study aimed to characterize the alteration of host reactive oxygen species (ROS) and OGG1 and to analyse the role of OGG1 in ASFV infection. We found that ASFV infection induced high levels and dynamic changes in ROS and 8-oxoG and consistently increased the expression of OGG1. Viral yield, transcription level, and protein synthesis were reduced in ASFV-infected primary alveolar macrophages (PAMs) treated by TH5487 or SU0268 inhibiting OGG1. The expression of BER pathway associated proteins of ASFV was also suppressed in OGG1-inhibited PAMs. Furthermore, OGG1 was found to negatively regulate interferon β (IFN-β) production during ASFV infection and IFN-β could be activated by OGG1 inhibition with TH5487 and SU0268, which blocked OGG1 binding to 8-oxoG. Additionally, the interaction of OGG1 with viral MGF360-14-L protein could disturb IFN-β production to further affect ASFV replication. These results suggest that OGG1 plays the crucial role in successful viral infection and OGG1 inhibitors SU0268 or TH5487 could be used as antiviral agents for ASFV infection.

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    OGG1 inhibition suppresses African swine fever virus replication

      Corresponding author: Qiaoying Zeng, zengqy@gsau.edu.cn
      Corresponding author: Qingli Niu, niuqingli@caas.cn
    • a. College of Veterinary Medicine, Gansu Agricultural University, Lanzhou, 730070, China;
    • b. African Swine Fever Regional Laboratory of China (Lanzhou), State Key Laboratory of Veterinary Etiological Biology, Key Laboratory of Veterinary Parasitology of Gansu Province, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, 730046, China;
    • c. Jiangsu Co-Innovation Center for the Prevention and Control of Important Animal Infectious Disease and Zoonosis, Yangzhou University, Yangzhou, 225009, China

    Abstract: African swine fever virus (ASFV) is an important pathogen that causes a highly contagious and lethal disease in swine, for which neither a vaccine nor treatment is available. The DNA repair enzyme 8-oxoguanine DNA glycosylase 1 (OGG1), which excises the oxidative base lesion 8-oxo-7,8-dihydroguanine (8-oxoG), has been linked to the pathogenesis of different diseases associated with viral infections. However, the role of OGG1-base excision repair (BER) in ASFV infection has been poorly investigated. Our study aimed to characterize the alteration of host reactive oxygen species (ROS) and OGG1 and to analyse the role of OGG1 in ASFV infection. We found that ASFV infection induced high levels and dynamic changes in ROS and 8-oxoG and consistently increased the expression of OGG1. Viral yield, transcription level, and protein synthesis were reduced in ASFV-infected primary alveolar macrophages (PAMs) treated by TH5487 or SU0268 inhibiting OGG1. The expression of BER pathway associated proteins of ASFV was also suppressed in OGG1-inhibited PAMs. Furthermore, OGG1 was found to negatively regulate interferon β (IFN-β) production during ASFV infection and IFN-β could be activated by OGG1 inhibition with TH5487 and SU0268, which blocked OGG1 binding to 8-oxoG. Additionally, the interaction of OGG1 with viral MGF360-14-L protein could disturb IFN-β production to further affect ASFV replication. These results suggest that OGG1 plays the crucial role in successful viral infection and OGG1 inhibitors SU0268 or TH5487 could be used as antiviral agents for ASFV infection.

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