Cellular microRNA miR-10a-5p inhibits replication of porcine reproductive and respiratory syndrome virus by targeting the host factor signal recognition particle 14
Zhao, Guangwei and Hou, Jianye and Xu, Gaoxiao and Xiang, Aoqi and Kang, Yanmei and Yan, Yunhuan and Zhang, Xiaobin and Yang, Gongshe and Xiao, Shuqi and Sun, Shiduo,, 98, 624-632 (2017),
doi = https://doi.org/10.1099/jgv.0.000708,
publicationName = Microbiology Society,
issn = 0022-1317,
abstract= Porcine reproductive and respiratory syndrome virus (PRRSV) is one of the most economically important viruses affecting the swine industry worldwide. MicroRNAs have recently been demonstrated to play vital roles in virus–host interactions. Our previous research on small RNA deep sequencing showed that the expression level of miR-10a increased during the viral life cycle. The present study sought to determine the function of miR-10a and its molecular mechanism during PRRSV infection. In the current study, the result of PRRSV infection inducing miR-10a expression was validated by quantitative reverse transcriptase PCR. Overexpression of miR-10a-5p using its mimics markedly reduced the expression level of intracellular PRRSV ORF7 mRNA and N protein. Simultaneously, overexpression of miR-10a-5p also significantly decreased the expression level of extracellular viral RNA and virus titres in the supernatants. These results demonstrated that miR-10a-5p could suppress the replication of PRRSV. A direct interaction between miR-10a-5p and signal recognition particle 14 (SRP14) was confirmed using bioinformatic prediction and experimental verification. miR-10a-5p could directly target the 3′UTR of pig SRP14 mRNA in a sequence-specific manner and decrease SRP14 expression through translational repression but not mRNA degradation. Further, knockdown of SRP14 by small interfering RNA also inhibits the replication of PRRSV. Collectively, these results suggested that miR-10a-5p inhibits PRRSV replication through suppression of SRP14 expression, which not only provides new insights into virus–host interactions during PRRSV infection but also suggests potential new antiviral strategies against PRRSV infection.,
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