Furusawa Yuri, Yamada Shinya, Kawaoka Yoshihiro
Division of Virology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, WI, United States.
Front Microbiol. 2018 Jul 24;9:1675. doi: 10.3389/fmicb.2018.01675. eCollection 2018.
Influenza virus replication relies on the functions of host factors. In our previous study, we identified host factors involved in virus replication and began analyses of their roles in this process. In this study, we focused on Nucleoporin 93 (NUP93) and revealed its importance in influenza virus replication. NUP93 knockdown mediated by siRNAs reduced viral replication and decreased the efficiency of the early step of the viral life cycle. NUP93 did not appear to be important for virus binding, internalization, or the nuclear import of viral ribonucleoprotein (vRNP); however, in NUP93-depleted cells, viral RNA accumulated in the nucleus. These results suggest that NUP93 is involved in the nuclear export of viral RNA.
流感病毒的复制依赖于宿主因子的功能。在我们之前的研究中，我们鉴定了参与病毒复制的宿主因子，并开始分析它们在此过程中的作用。在本研究中，我们聚焦于核孔蛋白93（NUP93），并揭示了其在流感病毒复制中的重要性。由小干扰RNA（siRNA）介导的NUP93敲低降低了病毒复制，并降低了病毒生命周期早期步骤的效率。NUP93似乎对病毒结合、内化或病毒核糖核蛋白（vRNP）的核输入不重要；然而，在NUP93缺失的细胞中，病毒RNA在细胞核中积累。这些结果表明，NUP93参与了病毒RNA的核输出。
