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Immune escape of bovine parvovirus by VP1 inhibiting IFN-β production through the RIG-I-like receptor pathway / Escape inmunológico del parvovirus bovino mediante la inhibición de VP1 de la producción de IFN-β a través de la vía del receptor tipo RIG-I
Zhuandi, Gong; Dianyu, Li; Mengyuan, Pei; Suocheng, Wei; Zhaofang, Yuan.
Afiliação
  • Zhuandi, Gong; Northwest Minzu University. Life Science and Engineering College. Lanzhou. China
  • Dianyu, Li; Northwest Minzu University. Life Science and Engineering College. Lanzhou. China
  • Mengyuan, Pei; Northwest Minzu University. Life Science and Engineering College. Lanzhou. China
  • Suocheng, Wei; Northwest Minzu University. Life Science and Engineering College. Lanzhou. China
  • Zhaofang, Yuan; Northwest Minzu University. Life Science and Engineering College. Lanzhou. China
Int. microbiol ; 26(4): 757-764, Nov. 2023. ilus, graf
Artigo em Inglês | IBECS | ID: ibc-227466
Biblioteca responsável: ES1.1
Localização: ES15.1 - BNCS
ABSTRACT

Objective:

The present study aimed to explore if bovine parvovirus (BPV) impacts beta interferon (IFN-β) production and to reveal further molecular mechanism of BPV immune escape.

Method:

The pCMV-Myc-BPV-VP1 recombinant plasmid was verified with both double-enzyme digestion and sequence. HEK 293 T cells were transfected with this recombinant protein and then infected with the vesicular stomatitis virus (VSV). Expression levels of IFN-β mRNA were detected using qPCR.

Results:

The expression level of BPV VP1 mRNA in the pCMV-Myc-BPV-VP1 group was significantly higher than those of the untreated group (UT) and pCMV-Myc vector group. BPV virus copies in bovine turbinate (BT) cells of the BPV-VP1 group were raised (P < 0.05) with an increment of 5.8 × 104. Expression levels of IFN-β mRNA of the BPV VP1 group in HEK 293 T cells were decreased (P < 0.01). Following treatment of TBK1 and IRF3(5D), IFN-β expression levels in HEK 293 T cells were depressed. Additionally, expression levels of TBK1, IRF3(5D), MDA5, and MAVS were less than those of the flag empty vector, respectively.

Conclusion:

pCMV-Myc-BPV-VP1 could heighten transcription levels of VP1 protein in BT cells, promote BPV proliferation, and ascend the production of IFN-β. Overexpression of pCMV-Myc-BPV-VP decreased IFN-β mRNA expression in HEK 293 T cells and inhibited IFN-β production induced by TBK1 and IRF3(5D). Furthermore, BPV VP1 obviously declined expression levels of TBK1, IRF3(5D), MDA5, and MAVS in the RIG-I-like receptor (RLR) pathway. Our findings revealed a novel mechanism evolved by BPV VP1 to inhibit type I IFN production and provided a solid scientific basis into the immunosuppression of BPV.(AU)
Assuntos

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Coleções: Bases de dados nacionais / Espanha Base de dados: IBECS Assunto principal: Técnicas Microbiológicas / Interferon beta / Bocavirus / Estomatite Vesicular / Microbiologia Limite: Humanos Idioma: Inglês Revista: Int. microbiol Ano de publicação: 2023 Tipo de documento: Artigo Instituição/País de afiliação: Northwest Minzu University/China
Buscar no Google
Coleções: Bases de dados nacionais / Espanha Base de dados: IBECS Assunto principal: Técnicas Microbiológicas / Interferon beta / Bocavirus / Estomatite Vesicular / Microbiologia Limite: Humanos Idioma: Inglês Revista: Int. microbiol Ano de publicação: 2023 Tipo de documento: Artigo Instituição/País de afiliação: Northwest Minzu University/China
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