猪源DDX56对口蹄疫病毒的复制及其对病毒诱导的RLR通路调节的研究

Porcine DDX56 Regulates the Foot and Mouth Disease Virus Replication and the Virus-triggered RLR Pathway

DEAD框解旋酶56(DDX56)是一种RNA解旋酶,能参与RNA代谢和核糖体的合成。为研究猪源DDX56对口蹄疫病毒(FMDV)复制和对病毒诱导的RLR通路的影响,首先通过免疫共沉淀试验筛选与猪源DDX56互作的FMDV蛋白;接着利用Q-PCR和Western blot检测过表达猪源DDX56对FMDV在PK-15细胞中复制的影响;然后利用双荧光素酶报告基因和Q-PCR检测猪源DDX56对病毒诱导的RLR通路的影响。结果显示,猪源DDX56能与FMDV蛋白VP0、VP1、VP2和3A发生相互作用;过表达猪源DDX56能够促进FMDV的复制;过表达猪源DDX56能抑制仙台病毒(SeV)诱导的RLR通路的激活;猪源DDX56可以协同FMDV蛋白VP0、VP1、VP2和3A抑制病毒诱导的Ⅰ型干扰素的产生。总之,猪源DDX56能与FMDV蛋白VP0、VP1、VP2和3A互作而协同抑制Ⅰ型干扰素的产生,从而促进FMDV的复制。

DEAD-box helicase 56(DDX56) belongs to the DEAD box helicase family that participate in RNA metabolism and ribosome synthesis. To study the effects of porcine DDX56 on replication of FMDV and virus-triggered RLR pathway, we screened the FMDV proteins for interacting with porcine DDX56. The effect of overexpression of porcine DDX56 on the replication of FMDV in PK-15 cells was detected by Q-PCR and Western blot experiments. The effect of porcine DDX56 on the virus-triggered RLR pathway was analyzed by double luciferase report system and Q-PCR assay. The results showed that porcine DDX56 interacts with FMDV VP0, VP1, VP2 and 3 A proteins. Overexpression of porcine DDX56 facilitated the replication of FMDV and inhibited the Sendai virus(SeV)-triggered activation of RLR pathway. Porcine DDX56 could cooperate with FMDV VP0, VP1, VP2 and 3 A proteins to inhibit the production of the virus-triggered type Ⅰ interferon. In a word, porcine DDX56 promotes the FMDV replication by cooperating with FMDV VP0, VP1, VP2 and 3 A proteins to inhibit the production of type Ⅰ interferon.