Insights into interactions between viral factors and the cellular machinery usually lead to discoveries concerning host cell biology. Thus, the gene expression field has historically relied on viral model systems to discover mechanisms underlying different cellular processes. In recent years, the functional characterization of the small nuclear noncoding RNAs expressed by the oncogenic Herpesvirus saimiri, called HSURs, resulted in the discovery of two mechanisms for the regulation of gene expression. HSUR1 and HSUR2 associate with host microRNAs, which are small noncoding RNAs that broadly regulate gene expression by binding to messenger RNAs. HSUR1 provided the first example of a process known as target-directed miRNA degradation that operates in cells to regulate miRNA populations. HSUR2 functions as a miRNA adaptor, uncovering an entirely new, indirect mechanism by which miRNAs can inhibit mRNA function. Here, I review the path that led to these discoveries and their implications and postulate new exciting questions about the functions of these fascinating viral noncoding RNAs.

深入了解病毒因子与细胞机制之间的相互作用通常会导致有关宿主细胞生物学的发现。因此，基因表达领域历来依赖病毒模型系统来发现不同细胞过程的机制。近年来，对致癌疱疹病毒 saimiri表达的小核非编码 RNA 的功能表征，HSURs，导致发现了两种调节基因表达的机制。HSUR1 和 HSUR2 与宿主 microRNA 相关联，它们是小的非编码 RNA，通过与信使 RNA 结合广泛调节基因表达。HSUR1 提供了第一个例子，该过程被称为靶标导向的 miRNA 降解，该过程在细胞中起作用以调节 miRNA 种群。HSUR2 充当 miRNA 接头，揭示了一种全新的间接机制，通过该机制 miRNA 可以抑制 mRNA 功能。在这里，我回顾了导致这些发现的路径及其影响，并假设关于这些迷人的病毒非编码 RNA 的功能的新问题。