Targeted knockout of Mx in the DF-1 chicken fibroblast cell line impairs immune response against Newcastle disease virus

Newcastle disease virus (NDV) is an RNA virus taking poultry as the host, and the Newcastle disease (ND) caused by NDV is one of the diseases with serious damage to the health of poultry. Mx encoding by myxovirus resistance gene, induced by type I interferon (IFN), has a wide range of antiviral and GTPase activi-ties in human, mice, and other species via inhibition virus replication. However, the antiviral ability of chicken Mx is still a controversial issue. To explore the effect of chicken Mx post-NDV infection, Mx-knockout DF-1 cells were constructed via CRISPR/Cas9 gene editing system. The number of copies of NDV was detected by RT-qPCR, and the mRNA expression levels of IRF-7, IFN-a, IFN-f3, TNF-a, p21, p27, and Bak in DF-1 cells were analyzed after NDV infection. Com-pared with control cells, virus titers were much higher in Mx-knockout DF-1 cells post-NDV infection. The defi-ciency of Mx aggravated the cell pathological features post-NDV infection, and promoted the expression levels of IRF-7, IFN-a, IFN-f3, and pro-inflammatory cytokine TNF-a in host cells. In addition, cells with Mx deficiency could alleviate the harm from virus by enhancing the expression of p21, p27, and Bak, which related to cell proliferation apoptosis. In conclusion, Mx played an important role in antivirus invasion. In the absence of Mx, cells could alleviate the harm from virus infection via retarding cell proliferation and enhancing cell apoptosis.

Automated summary

Newcastle disease virus (NDV) is an RNA virus that infects poultry, causing serious damage to their health. The role of chicken Mx in antivirus invasion is still controversial, but this study found that its deficiency resulted in higher virus titers and exacerbated cell pathological features post-NDV infection. The absence of Mx also led to increased expression levels of IRF-7, IFN-a, IFN-f3, and pro-inflammatory cytokine TNF-a, but it alleviated the harm from virus infection by enhancing the expression of p21, p27, and Bak, which are related to cell proliferation and apoptosis.