ACTA VETERINARIA ET ZOOTECHNICA SINICA ›› 2019, Vol. 50 ›› Issue (9): 1849-1856.doi: 10.11843/j.issn.0366-6964.2019.09.012

• PREVENTIVE VETERINARY MEDICINE • Previous Articles     Next Articles

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

FU Shaozu, LI Lulu, ZHANG Jing, LI Dan, ZHENG Haixue*   

  1. 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 730046, China
  • Received:2019-02-21 Online:2019-09-23 Published:2019-09-23

Abstract: 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 3A 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 3A 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 3A proteins to inhibit the production of type Ⅰ interferon.

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