Acta Veterinaria et Zootechnica Sinica ›› 2021, Vol. 52 ›› Issue (2): 450-459.doi: 10.11843/j.issn.0366-6964.2021.02.017

• PREVENTIVE VETERINARY MEDICINE • Previous Articles     Next Articles

Programmed Cell Death Factor 10 Inhibits Type Ⅰ Interferon Expression and Promotes the Replication of Foot-and-mouth Disease Virus

ZENG Zongbo1,2, MA Xusheng2, LUO Zhikuan2, QI Yayin1*, ZHENG Haixue2*   

  1. 1. College of Animal Science and Technology, Shihezi University, Shihezi 832000, China;
    2. State Key Laboratory of Veterinary Etiological Biology, National Foot-and-Mouth Disease Reference Laboratory, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou 730046, China
  • Received:2020-07-13 Online:2021-02-23 Published:2021-02-24

Abstract: The purpose of this study is to explore how the host protein programmed cell death factor 10 (PDCD10) can inhibit the expression of type Ⅰ interferon to promote the replication of foot-and-mouth disease virus (FMDV). First, this study verified the effect of overexpression and silencing of PDCD10 on FMDV replication. Secondly, the dual-luciferase reporter system was used to explore the effect of PDCD10 on the activation of type Ⅰ interferon signaling pathway. Finally, real-time fluorescent quantitative PCR was used to explore the effect of PDCD10 on the transcription of stimulating genes downstream of the type Ⅰ interferon pathway. The results showed that overexpression of PDCD10 significantly promoted FMDV replication while silencing PDCD10 significantly inhibited FMDV replication. Compared with the control, the cell culture supernatant infected with Sendai virus (SeV) after overexpression of PDCD10 significantly promoted FMDV replication. Furthermore, PDCD10 significantly inhibited the activation of IFN-β promoter and NF-κB induced by SeV in a dose-dependent manner, and PDCD10 negatively regulated the transcription of type Ⅰ interferon pathway signal molecules. Finally, it was found that PDCD10 negatively regulated the transcription of ISGs downstream of type Ⅰ interferon. The results of this study have accumulated data for the in-depth exploration of the role of PDCD10 in antiviral innate immunity.

Key words: programmed cell death factor 10, PDCD10, FMDV, Type Ⅰ interferon signaling pathway, IFN-β

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