In this study, the regulatory effect of the overexpression of polarity protein Lgl2 on the nuclear export of influenza A virus nucleoprotein in infected cells was investigated. A stable Tet-Off inducible MDCK cell line expressing a fusion protein comprising Lgl2 and an enhanced yellow fluorescent protein were used. TCID 50 analysis and neuraminidase activity analysis revealed that replication of influenza A virus was inhibited in Lgl2 overexpressing cells. By immunofluorescence microscopical observation at different time point post virus infection, a retention of NP in cellular nucleus was found in Lgl2 overexpressing cells. Compared with normal MDCK cells, change in claudin-1 distribution between cell contacts caused by Lgl2 overexpression impaired the barrier function of tight junction. These results suggest that changes in cell polarity induced by Lgl2 overexpressing will affect virus NP transportation.

中文翻译：

---

人细胞极性蛋白 Lgl2 调节甲型流感病毒核蛋白从 MDCK 细胞核中的输出

在这项研究中，研究了极性蛋白 Lgl2 过表达对感染细胞中甲型流感病毒核蛋白核输出的调节作用。使用稳定的 Tet-Off 诱导型 MDCK 细胞系，该细胞系表达包含 Lgl2 和增强型黄色荧光蛋白的融合蛋白。TCID 50 分析和神经氨酸酶活性分析表明，甲型流感病毒的复制在 Lgl2 过表达细胞中受到抑制。通过在病毒感染后不同时间点的免疫荧光显微镜观察，发现在 Lgl2 过表达细胞中 NP 保留在细胞核中。与正常 MDCK 细胞相比，由 Lgl2 过表达引起的细胞接触之间 claudin-1 分布的变化损害了紧密连接的屏障功能。