Fortes P, Lamond A I, Ortín J
Centro Nacional de Biotecnología (CSIC), Universidad Autonoma de Madrid, Cantoblanco, Spain.
J Gen Virol. 1995 Apr;76 ( Pt 4):1001-7. doi: 10.1099/0022-1317-76-4-1001.
Intranuclear structure was studied in influenza virus-infected cells by immunofluorescence microscopy with antibodies specific for fibrillarin, the splicing factor SC35 and the autoantigen p80 coilin. In the course of the infection, an increase in the number of coiled bodies was observed, with a parallel decrease in their size. In addition, the normal speckled pattern of the SC35 factor was altered to generate a more punctate distribution. However, no alteration was observed in the fibrillarin staining pattern. Since an alteration in the splicing of both viral and cellular mRNAs upon expression of influenza virus NS1 protein has been reported previously, the possible effects of NS1 expression on intranuclear structure were assayed. The increase in the coiled body numbers was not specific for the expression of NS1 protein, but alterations in the nuclear location of small ribonucleoprotein particles, as determined by immunofluorescence with an anti-Sm serum or the SC35 splicing factor, were produced by the sole expression of NS1 protein. These results correlate with the previously reported inhibition of splicing induced by NS1 protein expression and suggest an interaction of this influenza virus protein with the cellular splicing machinery.
利用针对纤维蛋白原、剪接因子SC35和自身抗原p80卷曲螺旋蛋白的特异性抗体,通过免疫荧光显微镜对流感病毒感染细胞的核内结构进行了研究。在感染过程中,观察到卷曲小体数量增加,其大小同时减小。此外,SC35因子正常的斑点状模式发生改变,形成更点状的分布。然而,纤维蛋白原的染色模式未观察到改变。由于先前已报道流感病毒NS1蛋白表达时病毒和细胞mRNA的剪接会发生改变,因此检测了NS1表达对核内结构的可能影响。卷曲小体数量的增加并非NS1蛋白表达所特有的,但通过抗Sm血清或SC35剪接因子的免疫荧光检测发现,NS1蛋白单独表达会导致小核糖核蛋白颗粒在核内位置的改变。这些结果与先前报道的NS1蛋白表达诱导的剪接抑制相关,并表明这种流感病毒蛋白与细胞剪接机制存在相互作用。