PDF(Pubmed)
Abstract：
Influenza virus infection poses a great threat to human health globally each year. Non-coding RNAs (ncRNAs) in the human genome have been reported to participate in the replication process of the influenza virus, among which there are still many unknowns about Long Intergenic Non-Coding RNAs (LincRNAs) in the cell cycle of viral infections. Here, we observed an increased expression of Linc01615 in A549 cells upon influenza virus PR8 infection, accompanied by the successful activation of the intracellular immune system. The knockdown of Linc01615 using the shRNAs promoted the proliferation of the influenza A virus, and the intracellular immune system was inhibited, in which the expressions of IFN-β, IL-28A, IL-29, ISG-15, MX1, and MX2 were decreased. Predictions from the catRAPID website suggested a potential interaction between Linc01615 and DHX9. Also, knocking down Linc01615 promoted influenza virus proliferation. The subsequent transcriptome sequencing results indicated a decrease in Linc01615 expression after influenza virus infection when DHX9 was knocked down. Further analysis through cross-linking immunoprecipitation and high-throughput sequencing (CLIP-seq) in HEK293 cells stably expressing DHX9 confirmed the interaction between DHX9 and Linc01615. We speculate that DHX9 may interact with Linc01615 to partake in influenza virus replication and that Linc01615 helps to activate the intracellular immune system. These findings suggest a deeper connection between DHX9 and Linc01615, which highlights the significant role of Linc01615 in the influenza virus replication process. This research provides valuable insights into understanding influenza virus replication and offers new targets for preventing influenza virus infections.
摘要：
流感病毒感染每年对全球人类健康构成巨大威胁。已报道人类基因组中的非编码RNA(ncRNAs)参与流感病毒的复制过程,其中，在病毒感染的细胞周期中，关于长基因间非编码RNA（LincRNA）仍然存在许多未知因素。这里,我们观察到流感病毒PR8感染后，在A549细胞中Linc01615的表达增加，伴随着细胞内免疫系统的成功激活。使用shRNA敲除Linc01615促进了甲型流感病毒的增殖，细胞内免疫系统受到抑制，其中IFN-β的表达，IL-28A,IL-29、ISG-15、MX1和MX2降低。来自catRAPID网站的预测表明Linc01615和DHX9之间存在潜在的相互作用。此外，敲除Linc01615促进流感病毒增殖。随后的转录组测序结果表明,当DHX9敲低时,流感病毒感染后Linc01615表达降低。通过稳定表达DHX9的HEK293细胞中的交联免疫沉淀和高通量测序（CLIP-seq）的进一步分析证实了DHX9和Linc01615之间的相互作用。我们推测DHX9可能与Linc01615相互作用以参与流感病毒的复制，而Linc01615有助于激活细胞内免疫系统。这些发现表明DHX9和Linc01615之间有更深层次的联系，这突出了Linc01615在流感病毒复制过程中的重要作用。这项研究为了解流感病毒复制提供了有价值的见解，并为预防流感病毒感染提供了新的靶标。
