ACTA VETERINARIA ET ZOOTECHNICA SINICA ›› 2018, Vol. 49 ›› Issue (12): 2664-2671.doi: 10.11843/j.issn.0366-6964.2018.12.015

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The Molecular Mechanism Study of miR-222 Inhibit Caprine Parainfluenza Virus Type 3 Replication

ZHONG Chun-yan1,3, LI Ji-zong1,2*, MAO Li1, LI Wen-liang1, HAO Fei1, SUN Min1, LIU Mao-jun1, ZHU Xing3, JI Xin-qin3, XIAO Fang1,3, YANG Lei-lei1, ZHANG Wen-wen1   

  1. 1. Key Laboratory of Veterinary Biological Engineering and Technology of Ministry of Agriculture, Institute of Veterinary Medicine, Jiangsu Academy of Agricultural Sciences, Nanjing 210014, China;
    2. School of Pharmacy, Linyi University, Linyi 276000, China;
    3. College of Animal Science of Guizhou University, Guiyang 550025, China
  • Received:2018-05-07 Online:2018-12-23 Published:2018-12-23

Abstract:

To explore the function of miR-222 on effecting the replication of caprine parainfluenza virus type 3 (CPIV3). The miR-222 mimics were synthesized and transfected into the MDBK cells, then infected with CPIV3. Twenty-four hours after infection, the cell cultures were harvested to determine the expression of CPIV3 genome and IFN mRNA. The molecular mechanism of effecting CPIV3 replication was explored using bioinformatics software, reporter gene system, RT-qPCR, Western blot and RNAi analysis. The results showed that the overexpression of miR-222 promote interferon (IFN) production to inhibit CPIV3 replication. Prediction the targets of miR-222 discovered that interferon regulatory factor 2 (IRF2) has a putative miR-222 target site and miR-222 mimics markedly decreased the luciferase level. Furthermore, transfection with miR-222 mimics decreased IRF2 expression in MDBK cells at both the mRNA and protein levels. Knockdown of miR-222 target inhibited CPIV3 replication. These findings indicate that overexpression of miR-222 promote the host antiviral innate immune response by targeting IRF2.

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