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4-Phenyl-butyric Acid Inhibits Japanese Encephalitis Virus Replication via Inhibiting Endoplasmic Reticulum Stress Response

文献类型： 外文期刊

作者： Wang, Shuangshuang 1 ; Yang, Keli 1 ; Li, Chang 1 ; Liu, Wei 1 ; Gao, Ting 1 ; Yuan, Fangyan 1 ; Guo, Rui 1 ; Liu, Zewen 1 ; Tan, Yiqing 1 ; Hu, Xianwang 1 ; Tian, Yongxiang 1 ; Zhou, Danna 1 ;

作者机构： 1.Inst Anim Husb & Vet, Hubei Acad Agr Sci, Key Lab Prevent & Control Agents Anim Bacteriosis, Hubei Prov Key Lab Anim Pathogen Microbiol,Minist, Wuhan 430064, Peoples R China

关键词： Japanese encephalitis virus; 4-PBA; UPR signaling pathway; non-structural protein 5

期刊名称：VIRUSES-BASEL （ 影响因子：4.7； 五年影响因子：4.8 ）

ISSN：

年卷期： 2023 年 15 卷 2 期

页码：

收录情况： SCI

摘要： Japanese encephalitis virus (JEV) infection causes host endoplasmic reticulum stress (ERS) reaction, and then induces cell apoptosis through the UPR pathway, invading the central nervous system and causing an inflammation storm. The endoplasmic reticulum stress inhibitor, 4-phenyl-butyric acid (4-PBA), has an inhibitory effect on the replication of flavivirus. Here, we studied the effect of 4-PBA on JEV infection both in vitro and vivo. The results showed that 4-PBA treatment could significantly decrease the titer of JEV, inhibit the expression of the JEV NS3 protein (in vitro, p < 0.01) and reduce the positive rate of the JEV E protein (in vivo, p < 0.001). Compared to the control group, 4-PBA treatment can restore the weight of JEV-infected mice, decrease the level of IL-1 beta in serum and alleviate the abnormalities in brain tissue structure. Endoplasmic reticulum stress test found that the expression level of GRP78 was much lower and activation levels of PERK and IRE1 pathways were reduced in the 4-PBA treatment group. Furthermore, 4-PBA inhibited the UPR pathway activated by NS3, NS4b and NS5 RdRp. The above results indicated that 4-PBA could block JEV replication and inhibit ER stress caused by JEV. Interestingly, 4-PBA could reduce the expression of NS5 by inhibiting transcription (p < 0.001), but had no effect on the expression of NS3 and NS4b. This result may indicate that 4-PBA has antiviral activity independent of the UPR pathway. In summary, the effect of 4-PBA on JEV infection is related to the inhibition of ER stress, and it may be a promising drug for the treatment of Japanese encephalitis.

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