Influenza B virus (IBV) is a respiratory pathogen that infects humans and causes seasonal influenza epidemics. However, cellular response to IBV infection in humans and mechanisms of host-mediated restriction of IBV replication are not thoroughly understood. In this study, we used next-generation sequencing (NGS) to perform transcriptome profiling of IBV-infected human lung epithelial A549 cells at 0, 6, 12, and 24 h post infection (hpi) and characterized the cellular gene expression dynamics. We observed that more than 4000 host genes were differentially regulated during the study period, which included up regulation of genes encoding proteins, having a role in the innate antiviral immune responses, immune activation, cellular metabolism, autophagy, and apoptosis, as well as down regulation of genes involved in mitosis and cell proliferation. Further analysis of RNA-Seq data coupled with RT-qPCR validation collectively showed that double-strand RNA recognition pathways, including retinoic acid-inducible gene I (RIG-I) and Toll-like receptor 3 (TLR3), were substantially activated following IBV infection. Taken together, these results provide important initial insights into the intimate interaction between IBV and lung epithelial cells, which can be further explored towards elucidation of the cellular mechanisms in restriction or elimination of IBV infections in humans.

中文翻译：

---

细胞对乙型流感病毒感染的反应的下一代测序分析。

乙型流感病毒（IBV）是一种呼吸道病原体，可感染人类并引起季节性流感流行。然而，人类对IBV感染的细胞应答和宿主介导的IBV复制限制的机制尚未完全了解。在这项研究中，我们使用下一代测序（NGS）在感染后（hpi）0、6、12和24 h对IBV感染的人肺上皮A549细胞进行转录组分析，并表征了细胞基因表达动态。我们观察到在研究期间，有4000多个宿主基因受到差异调节，其中包括编码蛋白的基因上调，在先天抗病毒免疫反应，免疫激活，细胞代谢，自噬和凋亡以及下调中起作用。调控参与有丝分裂和细胞增殖的基因。进一步的RNA-Seq数据分析和RT-qPCR验证共同表明，IBV后基本上激活了双链RNA识别途径，包括视黄酸诱导基因I（RIG-1）和Toll样受体3（TLR3）。感染。综上所述，这些结果为IBV与肺上皮细胞之间的紧密相互作用提供了重要的初步见识，可以进一步探索阐明限制或消除人类IBV感染的细胞机制。