Brunetti Jesús E, Scolaro Luis A, Castilla Viviana
Laboratorio de Virología, Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Ciudad Universitaria, Pabellón 2, Piso 4, Ciudad Autónoma de Buenos Aires, C1428EGA, Argentina.
Laboratorio de Virología, Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Ciudad Universitaria, Pabellón 2, Piso 4, Ciudad Autónoma de Buenos Aires, C1428EGA, Argentina.
Virus Res. 2015 May 4;203:84-91. doi: 10.1016/j.virusres.2015.04.001. Epub 2015 Apr 10.
Heterogeneous nuclear ribonucleoproteins (hnRNPs) are cellular factors involved in the replication of several viruses. In this study we analyzed the expression and intracellular localization of hnRNP A2 and hnRNP K in cell cultures infected with two viruses that cause human hemorrhagic fevers: dengue virus type 2 (DENV-2) and Junín virus (JUNV). We determined that DENV-2 promoted the cytoplasmic translocation of hnRNP K and to a lesser extent of hnRNP A2, meanwhile, JUNV infection induced an increase in hnRNP K cytoplasmic localization whereas hnRNP A2 remained mainly in the nucleus of infected cells. Both hnRNP K and hnRNP A2 were localized predominantly in the nucleus of JUNV persistently-infected cells even after superinfection with JUNV indicating that persistent infection does not alter nucleo-cytoplasmic transport of these hnRNPs. Total levels of hnRNP K expression were unaffected by DENV-2 or JUNV infection. In addition we determined, using small interfering RNAs, that hnRNP K knockout inhibits DENV-2 and JUNV multiplication. Our results indicate that DENV-2 and JUNV induce hnRNP K cytoplasmic translocation to favor viral multiplication.
不均一核核糖核蛋白（hnRNPs）是参与多种病毒复制的细胞因子。在本研究中，我们分析了hnRNP A2和hnRNP K在感染两种引起人类出血热病毒的细胞培养物中的表达和细胞内定位：2型登革病毒（DENV-2）和胡宁病毒（JUNV）。我们确定DENV-2促进hnRNP K的细胞质转位，对hnRNP A2的促进作用较小，同时，JUNV感染导致hnRNP K细胞质定位增加，而hnRNP A2主要保留在受感染细胞的细胞核中。即使在JUNV再次感染后，hnRNP K和hnRNP A2在JUNV持续感染细胞中仍主要定位于细胞核，这表明持续感染不会改变这些hnRNPs的核质运输。hnRNP K的总表达水平不受DENV-2或JUNV感染的影响。此外，我们使用小干扰RNA确定，敲除hnRNP K可抑制DENV-2和JUNV的增殖。我们的结果表明，DENV-2和JUNV诱导hnRNP K细胞质转位以促进病毒增殖。
