Virus Laboratory, the Affiliated Shengjing Hospital, China Medical University, Shenyang 110004, China.
FEBS Lett. 2013 Jul 11;587(14):2266-71. doi: 10.1016/j.febslet.2013.05.057. Epub 2013 Jun 6.
It has been reported that human cytomegalovirus (HCMV) miR-US25-2 reduces DNA viral replication including HCMV. However, the mechanism remains unknown. In our study, eukaryotic translation initiation factor 4A1 (eIF4A1) was identified to be a direct target of miR-US25-2-3p. Small interfering RNA (siRNA) and miR-US25-2-3p mediated eIF4A1 knockdown experiments revealed that high level of miR-US25-2-3p in MRC-5 cells decreased HCMV and host genomic DNA synthesis, and inhibited cap-dependent translation and host cell proliferation. However, eIF4A1 up-regulation induced by miR-US25-2-3p inhibitor increased HCMV copy number. Therefore, the over-expression of miR-US25-2-3p and consequent lower expression of eIF4A1 may contribute to the inhibition of HCMV replication.
据报道,人巨细胞病毒 (HCMV) miR-US25-2 可降低包括 HCMV 在内的 DNA 病毒复制。然而,其机制尚不清楚。在我们的研究中,真核翻译起始因子 4A1 (eIF4A1) 被鉴定为 miR-US25-2-3p 的直接靶标。小干扰 RNA (siRNA) 和 miR-US25-2-3p 介导的 eIF4A1 敲低实验表明,MRC-5 细胞中高水平的 miR-US25-2-3p 可降低 HCMV 和宿主基因组 DNA 合成,并抑制帽依赖翻译和宿主细胞增殖。然而,miR-US25-2-3p 抑制剂诱导的 eIF4A1 上调增加了 HCMV 拷贝数。因此,miR-US25-2-3p 的过表达和随之而来的 eIF4A1 表达降低可能有助于抑制 HCMV 复制。