Journal
VIRUSES-BASEL
Volume 14, Issue 10, Pages -Publisher
MDPI
DOI: 10.3390/v14102225
Keywords
DF-1; CRISPR; Cas9; IFNAR1; duck Tembusu virus; transcriptomic analysis
Categories
Funding
- Independent project of Zhaoqing Branch Center of Guangdong Laboratory for Lingnan Modern Agricultural Science and Technology [P202111540301, P20211154-0202]
- Zhaoqing Science Foundation of China [2019K040, 2020NCP0102]
- Guangdong Province Key Field RD Program [2021B0707010009]
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This study reports the construction of a DF-1 cell line with knockout IFNAR1 gene, which enhances the replication of DTMUV and activates genes and signaling pathways related to cell growth and apoptosis. Knockdown of two up-regulated genes, HELZ2 and IFI6, also increases the replication of DTMUV RNA.
For industrial vaccine production, overwhelming the existing antiviral innate immune response dominated by type I interferons (IFN-I) in cells would be a key factor improving the effectiveness and production cost of vaccines. In this study, we report the construction of an IFN-I receptor 1 (IFNAR1)-knockout DF-1 cell line (KO-IFNAR1), which supports much more efficient replication of the duck Tembusu virus (DTMUV), Newcastle disease virus (NDV) and gammacoronavirus infectious bronchitis virus (IBV). Transcriptomic analysis of DTMUV-infected KO-IFNAR1 cells demonstrated that DTMUV mainly activated genes and signaling pathways related to cell growth and apoptosis. Among them, JUN, MYC and NFKBIA were significantly up-regulated. Furthermore, knockdown of zinc-fingered helicase 2 (HELZ2) and interferon-alpha-inducible protein 6 (IFI6), the two genes up-regulated in both wild type and KO-IFNAR1 cells, significantly increased the replication of DTMUV RNA. This study paves the way for further studying the mechanism underlying the DTMUV-mediated IFN-I-independent regulation of virus replication, and meanwhile provides a potential cell resource for efficient production of cell-based avian virus vaccines.
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