Viral infection induces the expression of numerous host genes that impact the outcome of infection. Here we show that infection of human lung epithelial cells with Influenza A virus (IAV) also induces a broad program of alternative splicing of host genes. While these splicing-regulated genes are not enriched for canonical regulators of viral infection, we find that many of these genes do impact replication of IAV. Moreover, specific inhibition of the IAV-induced splicing in several cases also attenuates viral infection. We further show that approximately a quarter of the IAV-induced splicing events are regulated by hnRNP K, a host protein that required for efficient splicing of the IAV M transcript in nuclear speckles. Notably, we find that hnRNP K accumulates in nuclear speckles upon IAV infection, which is likely to alter the accessibility of hnRNP K for host transcripts thereby leading to a program of host splicing changes that promote IAV replication.

中文翻译：

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病毒诱导的宿主基因的选择性剪接促进流感复制。

病毒感染会诱导许多宿主基因的表达，从而影响感染的结果。在这里，我们显示，用A型流感病毒（IAV）感染人肺上皮细胞也会诱导宿主基因的选择性剪接的广泛程序。虽然这些剪接调节的基因没有丰富病毒感染的规范性调节剂，但我们发现许多这些基因确实影响了IAV的复制。而且，在几种情况下，对IAV诱导的剪接的特异性抑制也减弱了病毒感染。我们进一步显示，大约有四分之一的IAV诱导的剪接事件受hnRNP K调控，hnRNP K是在核斑点中有效剪接IAV M转录本所需的宿主蛋白。值得注意的是，我们发现IAR感染后hnRNP K累积在核斑中，