基因敲除
生物
病毒复制
小RNA
核糖核酸
基因
下调和上调
病毒
病毒学
细胞生物学
分子生物学
遗传学
作者
Juan Huang,Lin Liu,Min Cui,Anchun Cheng,Mingshu Wang,Mafeng Liu,Dekang Zhu,Shun Chen,Xinxin Zhao,Qiao Yang,Ying Wu,Shaqiu Zhang,Xumin Ou,Sai Mao,Qun Gao,Dan Sun,Bin Tian,Zhongqiong Yin,Renyong Jia
标识
DOI:10.1016/j.psj.2023.102890
摘要
Duck Tembusu Virus (DTMUV), belonging to the Flaviviridae family, is a major virus that affects duck health in China. MicroRNAs (miRNAs) play a important role in viral replication. However, little is known about the function of miRNAs during DTMUV infection. Here, the host miR-146b-5p was found to regulate DTMUV replication. When DTMUV infected duck embryo fibroblasts (DEFs), the expression levels of miR-146b-5p increased significantly over time. Moreover, the viral RNA copies, E protein expression levels and virus titers were all upregulated when miR-146b-5p was overexpressed in DEFs. The opposite results were also observed upon knockdown of miR-146b-5p in DEFs. To explore the mechanism by which miR-146b-5p promoted DTMUV replication, mass spectrometry and RNA pull-down assays were employed. Ribosomal protein S14 (RPS14), a component of 40S ribosomal proteins, was identified to interact with miR-146b-5p. In addition, the relative mRNA expression levels of RPS14 gene were negatively modulated by miR-146b-5p. Subsequently, it was found that overexpression of RPS14 could decrease the replication of DTMUV, and the reverse results were also detected by knockdown of RPS14. In conclusion, this study revealed that miR-146b-5p promoted DTMUV replication by targeting RPS14, which provides a new mechanism by which DTMUV evades host defenses and a new direction for further antiviral strategies development.
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