Whittaker G, Bui M, Helenius A
Department of Cell Biology, Yale University School of Medicine, New Haven, Connecticut, USA.
J Virol. 1996 May;70(5):2743-56. doi: 10.1128/JVI.70.5.2743-2756.1996.
The influenza virus nucleoprotein (NP), matrix protein (M1), and ribonucleoproteins (vRNPs) undergo regulated nuclear import and export during infection. Their trafficking was analyzed by using interspecies heterokaryons containing nuclei from infected and uninfected cells. Under normal conditions, it was demonstrated that the vRNPs which were assembled in the nucleus and transported to the cytosol were prevented from reimport into the nucleus. To be import competent, they must first assemble into virions and enter by the endosomal entry pathway. In influenza virus mutant ts51, in which M1 is defective, direct reimport took place but was inhibited by heterologous expression of wild-type M1. These data confirm M1's role as the inhibitor of premature nuclear import and as the main regulator of nuclear transport of vRNPs. In addition to this vRNP shuttling, M1 also shuttled between the nucleus and the cytoplasm in ts51-infected cells. When NP was expressed in the absence of virus infection, it was also found to be a shuttling protein.
流感病毒核蛋白（NP）、基质蛋白（M1）和核糖核蛋白（vRNP）在感染过程中经历受调控的核输入和输出。通过使用含有感染细胞和未感染细胞细胞核的种间异核体来分析它们的运输。在正常情况下，已证明在细胞核中组装并转运到细胞质中的vRNP被阻止重新输入细胞核。为了具备输入能力，它们必须首先组装成病毒粒子并通过内体进入途径进入。在M1有缺陷的流感病毒突变体ts51中，发生了直接重新输入，但受到野生型M1异源表达的抑制。这些数据证实了M1作为过早核输入抑制剂和vRNP核运输主要调节因子的作用。除了这种vRNP穿梭外，M1在ts51感染的细胞中也在细胞核和细胞质之间穿梭。当在没有病毒感染的情况下表达NP时，也发现它是一种穿梭蛋白。
