Poly (rC) binding protein 2 interacts with VP0 and increases the replication of the foot-and-mouth disease virus
Poly (rC) binding protein 2 interacts with VP0 and increases the replication of the foot-and-mouth disease virus
复制标题
Poly (rC) 结合蛋白 2 与 VP0 相互作用并增加口蹄疫病毒的复制
DOI：
10.1038/s41419-019-1751-6
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发表时间：
2019-07-04
影响因子：
9
通讯作者：
Zheng, Haixue
中科院分区：
文献类型：
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作者：
Li, Dan;Zhang, Jing;Zheng, Haixue
口蹄疫病毒（FMDV）是一种传染性极强的致偶蹄类动物衰弱性疾病，可导致毁灭性的经济后果。以往的研究报道，一些口蹄疫病毒蛋白可以与宿主蛋白相互作用，影响口蹄疫病毒的复制。然而，FMDV VP 0蛋白与其配偶体之间的相互作用对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（PCBP 2）的过表达促进FMDV的复制，而PCBP 2的敲低抑制FMDV的复制。PCBP 2还可与FMDV VP 0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 VP 0蛋白增强了PCBP 2-VISA复合物的形成。最终，我们发现，VISA的降解在PCBP 2敲低和FMDV VP 0过表达的细胞或FMDV VP 0敲低的细胞中比在对照细胞中更弱。综上所述，我们的数据显示PCBP 2和VP 0之间的相互作用可以通过凋亡途径促进FMDV的复制。
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.