State Key Laboratory of Veterinary Etiological Biology and OIE/National Foot and Mouth Disease Reference Laboratory, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, Gansu, China.
Cell Death Dis. 2019 Jul 4;10(7):516. doi: 10.1038/s41419-019-1751-6.
Foot-and-mouth disease virus (FMDV) causes a highly contagious and debilitating disease in cloven-hoofed animals, which leads to devastating economic consequences. Previous studies have reported that some FMDV proteins can interact with host proteins to affect FMDV replication. However, the influence of the interactions between FMDV VP0 protein and its partners on FMDV replication remains unknown. In this study, we found that the overexpression of poly (rC) binding protein 2 (PCBP2) promoted FMDV replication, whereas the knockdown of PCBP2 suppressed FMDV replication. Furthermore, PCBP2 can interact with FMDV VP0 protein to promote the degradation of VISA via the apoptotic pathway. Further studies demonstrated that FMDV VP0 protein enhanced the formation of the PCBP2-VISA complex. Ultimately, we found that the degradation of VISA was weaker in PCBP2-knockdown and FMDV VP0-overexpressing cells, or FMDV VP0-knockdown cells than in the control cells. Summarily, our data revealed that the interaction between PCBP2 and VP0 could promote FMDV replication via the apoptotic pathway.
口蹄疫病毒(FMDV)会导致偶蹄类动物发生高度传染性和使人虚弱的疾病,从而造成毁灭性的经济后果。先前的研究报告称,一些 FMDV 蛋白可以与宿主蛋白相互作用,从而影响 FMDV 的复制。然而,FMDV VP0 蛋白与其伙伴之间相互作用对 FMDV 复制的影响尚不清楚。在这项研究中,我们发现多聚(rC)结合蛋白 2(PCBP2)的过表达促进了 FMDV 的复制,而 PCBP2 的敲低则抑制了 FMDV 的复制。此外,PCBP2 可以与 FMDV VP0 蛋白相互作用,通过凋亡途径促进 VISA 的降解。进一步的研究表明,FMDV VP0 蛋白增强了 PCBP2-VISA 复合物的形成。最终,我们发现与对照细胞相比,在 PCBP2 敲低和 FMDV VP0 过表达的细胞或 FMDV VP0 敲低的细胞中,VISA 的降解较弱。总之,我们的数据表明 PCBP2 和 VP0 之间的相互作用可以通过凋亡途径促进 FMDV 的复制。