猪瘟病毒研究新进展
猪瘟病毒(CSFV)非结构蛋白NS5A是一种多功能蛋白,其能够调节病毒的基因组复制,蛋白质翻译及与宿主细胞的相互作用的蛋白。热休克蛋白27(Hsp27)属于低分子量热休克安白家族的成员,是一个涉及到药物抗性、细胞生长、细胞凋亡等功能的重要蛋白。近日,中国的科学家通过将PK-15细胞的Hsp27蛋白使用siRNA的方法沉默和上调发现,当该蛋白沉默时,CSFV的增殖能力增强;当该蛋白表达量上升时,CSFV的病毒增殖受到抑制。与此同时,科学家们还发现在Hsp27上调时,能够增强NF-kB信号通路。在Hsp27上调时,通过抑制NF-kB信号通路,能够消除CSFV的增殖抑制。试验结果充分证实,Hsp27对CSFV增殖的抑制作用是通过NF-kB信号通路实现的。该研究成功已在线发表至Virology杂志,文章题为“Cellular Hsp27 interacts with classical swine fever virus NS5Aprotein and negatively regulates viral replication by the NF-kB signalingpathway”。原文摘要:
Classical swine fever virus (CSFV) nonstructural protein NS5A is a multifunctional protein functioning in regulation of viral genome replication, protein translation and assembly by interaction with viral or host proteins. Here, heat shock protein 27 (Hsp27) has been identified as a novel binding partner of NS5A by using His tag “pull down” coupled with shotgun LC-MS/MS, with interaction of both proteins further confirmed by co-immunoprecipitation and laser confocal assays. In PK-15 cells, silencing of Hsp27 expression by siRNA enhanced CSFV replication, and upregulation of Hsp27 inhibited viral proliferation. Additionally, we have shown that overexpression of Hsp27 increased NF-κB signaling induced by TNFα. Blocking NF-κB signaling in PK-15 cells overexpressing Hsp27 by ammonium pyrrolidinedithiocarbamate (PDTC) eliminated the inhibition of CSFV replication by Hsp27. These findings clearly demonstrate that the inhibition of CSFV replication by Hsp27 is mediated via the NF-κB signaling pathway.
文章链接:https://www.sciencedirect.com/science/article/pii/S0042682218300643
页:
[1]