ABSTRACT
Objective: To investigate the effect of type I interferon receptor 1 (IFNAR1) on Pseudorabies virus (PRV) replication. Methods: A stable cell line in which porcine kidney epithelial cells (PK 15) knocked out the IFNAR1 gene was constructed using a lentiviral-mediated CRISPR/Cas9 (clustered regularly interspaced short palindromic repeats, CRISPR) gene editing technique. The function of IFNAR1 was verified by cell viability assay, fluorescence observation, flow cytometry detection, titer determination, and Real-time PCR. Results: With the prolongation of PRV infection, knocking out the IFNAR1 gene can significantly promote transcription of PRV-TK mRNA, translation of PRV-gE protein, and virulence of progeny virus. Conclusion: IFNAR1 plays an important role in inhibiting the proliferation of PRV.