Immune escape of bovine parvovirus by VP1 inhibiting IFN-β production through the RIG-I-like receptor pathway

  • Int Microbiol. 2023 Jan 27;1-8. doi: 10.1007/s10123-023-00330-8.
Gong Zhuandi  1 ,  Yuan Zhaofang  2 ,  Li Dianyu  2  3 ,  Pei Mengyuan  2 ,  Wei Suocheng  4  5
Affiliations
  • 1. Hospital, Northwest Minzu University, Lanzhou, 730030, China.
  • 2. Life Science and Engineering College, Northwest Minzu University, Lanzhou, 730030, China.
  • 3. Lanzhou Baiyuan Gene Technology Co., Ltd., No. 102, Yandong Road, Chengguan District, 730030, Lanzhou, China.
  • 4. Life Science and Engineering College, Northwest Minzu University, Lanzhou, 730030, China. [email protected].
  • 5. Lanzhou Baiyuan Gene Technology Co., Ltd., No. 102, Yandong Road, Chengguan District, 730030, Lanzhou, China. [email protected].
PMID: 36703013 DOI: 10.1007/s10123-023-00330-8
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.

Keywords
Bovine parvovirus; IFN-β; RIG-I-like receptor; VP1 protein.
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