Neuraminidase (NA) is an integral membrane protein of influenza A virus (IAV) and primarily aids in the release of progeny virions, following the intracellular viral replication cycle. In an attempt to discover new functions of NA, we conducted a classical yeast two‐hybrid screen and found acute myeloid leukaemia marker 1 (AML1) as a novel interacting partner of IAV‐NA. The interaction was further validated by co‐immunoprecipitation in IAV‐infected cells and in an in vitro coupled transcription/translation system. Interestingly, we found an increase in the expression of AML1 upon IAV infection in a dose‐dependent manner. As expected, we also observed an increase in the IFN‐β levels, the first line of defence against viral infections. Subsequently, when AML1 was downregulated using siRNA, the IFN‐β levels were found to be remarkably reduced. Our study also shows that AML1 is induced upon IAV infection and results in the induction of IFN‐β. Thus, AML1 is proposed to be an important player in IFN induction and has a role in an antiviral response against IAV infection.

中文翻译：

---

AML1 蛋白与甲型流感病毒神经氨酸酶相互作用并上调受感染哺乳动物细胞中的 IFNβ 反应

神经氨酸酶 (NA) 是甲型流感病毒 (IAV) 的完整膜蛋白，主要有助于在细胞内病毒复制周期后释放子代病毒粒子。为了发现 NA 的新功能，我们进行了经典的酵母双杂交筛选，发现急性髓系白血病标记物 1（AML1）是 IAV-NA 的新型相互作用伙伴。通过 IAV 感染细胞中的免疫共沉淀和体外偶联转录/翻译系统进一步验证了这种相互作用。有趣的是，我们发现 IAV 感染后 AML1 的表达以剂量依赖性方式增加。正如预期的那样，我们还观察到 IFN-β 水平的增加，这是抵御病毒感染的第一道防线。随后，当使用 siRNA 下调 AML1 时，发现 IFN-β 水平显着降低。我们的研究还表明 AML1 在 IAV 感染后被诱导并导致 IFN-β 的诱导。因此，AML1 被认为是 IFN 诱导的重要参与者，并在针对 IAV 感染的抗病毒反应中发挥作用。