Partial antiviral activities of the Asn631 chicken Mx against newcastle disease virus and vesicular stomatitis virus
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  • 作者:Bichun Li (1) yubcli@yzu.edu.cn
    Dezhi Fu (1)
    Yani Zhang (1)
    Qi Xu (1)
    Ligang Ni (1)
    Guobin Chang (1)
    Mengmeng Zheng (1)
    Bo Gao (1)
    Huaichang Sun (2)
    Guohong Chen (1) ghchen@yzu.edu.cn
  • 关键词:Chicken Mx &#8211 ; cDNA variants &#8211 ; Antiviral activity &#8211 ; NDV &#8211 ; VSV
  • 刊名:Molecular Biology Reports
  • 出版年:2012
  • 出版时间:August 2012
  • 年:2012
  • 卷:39
  • 期:8
  • 页码:8415-8424
  • 全文大小:1.0 MB
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  • 作者单位:1. College of Animal Science and Technology, Yangzhou University, Yangzhou, 225009 People鈥檚 Republic of China2. College of Veterinary Medicine, Yangzhou University, Yangzhou, 225009 People鈥檚 Republic of China
  • ISSN:1573-4978
文摘
Conflicting data existed for the antiviral potential of the chicken Mx protein and the importance of the Asn631 polymorphism in determination of the antiviral activity. In this study we modified the chicken Mx cDNA from the Ser631 to Asn631 genotype and transfected them into COS-I cells, chicken embryonic fibroblast (CEF) or NIH 3T3 cells. The Mx protein was mainly located at the cytoplasm. The transfected cell cultures were challenged with newcastle disease virus (NDV) or vesicular stomatitis virus (VSV), cytopathic affect (CPE) inhibition assay showed that the times for development of visible and full CPE were significantly postponed by the Asn631 cDNA transfection at 48 h transfection, but not by the Ser631 cDNA transfection. Viral titration assay showed that the virus titers were significantly reduced before 72 h postinfection. CEF cells was incubated by the cell lysates extracted from the COS-I cells transfected with pcDNA-Mx/Asn631, could resist and delayed NDV infection. These data suggested the importance of the Asn631 polymorphism of the chicken Mx in determination of the antiviral activities against NDV and VSV at early stage of viral infection, which were relatively weak and not sufficient to inhibit the viral replication at late stage of viral infection.
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