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首页> 外文期刊>EMBO reports >MicroRNAs encoded by Kaposi's sarcoma-associated herpesvirus regulate viral life cycle
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MicroRNAs encoded by Kaposi's sarcoma-associated herpesvirus regulate viral life cycle

机译：卡波西氏肉瘤相关疱疹病毒编码的MicroRNA调节病毒的生命周期

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摘要

Kaposi's sarcoma-associated herpesvirus (KSHV) is linked with Kaposi's sarcoma and lymphomas. The pathogenesis of KSHV depends on the balance between two phases of the viral cycle: latency and lytic replication. In this study, we report that KSHV-encoded microRNAs (miRNAs) function as regulators by maintaining viral latency and inhibiting viral lytic replication. MiRNAs are short, noncoding, small RNAs that post-transcriptionally regulate the expression of messenger RNAs. Of the 12 viral miRNAs expressed in latent KSHV-infected cells, we observed that expression of miR-K3 can suppress both viral lytic replication and gene expression. Further experiments indicate that miR-K3 can regulate viral latency by targeting nuclear factor I/B. Nuclear factor I/B can activate the promoter of the viral immediate-early transactivator replication and transcription activator (RTA), and depletion of nuclear factor I/B by short hairpin RNAs had similar effects on the viral life cycle to those of miR-K3. Our results suggest a role for KSHV miRNAs in regulating the viral life cycle.
机译：卡波西氏肉瘤相关疱疹病毒（KSHV）与卡波西氏肉瘤和淋巴瘤相关。 KSHV的发病机理取决于病毒周期两个阶段之间的平衡：潜伏期和裂解复制。在这项研究中，我们报告说，通过保持病毒潜伏期和抑制病毒裂解复制，KSHV编码的microRNA（miRNA）发挥了调节作用。 MiRNA是短的，非编码的小RNA，可在转录后调节信使RNA的表达。在潜伏的KSHV感染细胞中表达的12种病毒miRNA中，我们观察到miR-K3的表达可以抑制病毒裂解复制和基因表达。进一步的实验表明，miR-K3可以通过靶向核因子I / B来调节病毒潜伏期。核因子I / B可以激活病毒立即早期反式激活因子复制和转录激活剂（RTA）的启动子，而短发夹RNA耗尽核因子I / B对病毒生命周期的影响与miR-K3类似。我们的结果表明KSHV miRNA在调节病毒生命周期中的作用。

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