Guo Xin, Qi Ying, Huang Yujing, Liu Zhongyang, Ma Yanping, Shao Yaozhong, Jiang Shujuan, Sun Zhengrong, Ruan Qiang
Virus Laboratory, Affiliated Shengjing Hospital, China Medical University, Shenyang, Liaoning 110004, China.
Virus Laboratory, Affiliated Shengjing Hospital, China Medical University, Shenyang, Liaoning 110004, China.
FEBS Lett. 2015 Feb 13;589(4):440-6. doi: 10.1016/j.febslet.2014.12.030. Epub 2015 Jan 10.
During infection with human cytomegalovirus (HCMV), overexpression of hcmv-miR-US33 can inhibit the lytic viral replication and down-regulate US29 mRNA. However, it remains unknown whether inhibition of viral replication by miR-US33 is mediated by down-regulation of expression of US29 or another host gene. Here, we identified the host gene Syntaxin3 (STX3) to be a direct target of hcmv-miR-US33-5p using Hybrid-PCR and luciferase-reporter assays. It was further demonstrated that the levels of STX3 protein were down-regulated in hcmv-miR-US33-5p-overexpressing cells. Experiments with STX3-specific siRNA, or with an inhibitor of hcmv-miR-US33-5p confirmed that hcmv-miR-US33-5p-mediated inhibition of HCMV DNA synthesis and of viral replication are specifically mediated by down-regulation of STX3 expression.
在人巨细胞病毒（HCMV）感染期间，hcmv-miR-US33的过表达可抑制病毒的裂解复制并下调US29 mRNA。然而，miR-US33对病毒复制的抑制作用是否由US29或其他宿主基因表达的下调介导仍不清楚。在此，我们使用杂交PCR和荧光素酶报告基因检测法，确定宿主基因Syntaxin3（STX3）是hcmv-miR-US33-5p的直接靶点。进一步证明，在过表达hcmv-miR-US33-5p的细胞中，STX3蛋白水平下调。使用STX3特异性siRNA或hcmv-miR-US33-5p抑制剂进行的实验证实，hcmv-miR-US33-5p介导的对HCMV DNA合成和病毒复制的抑制作用是由STX3表达的下调特异性介导的。
