Preliminary Study Of Prenylcysteine Oxidase 1 Regulating Viral Infection

Explore the effect of Prenylcysteine Oxidase 1 (PCYOX1) on vesicular stomatitis virus (VSV) replication and innate type I interferon response. The small interfering RNA or plasmid was transfected to knock down or overexpress PCYOX1 gene in BJ-5ta cells. After infecting cells with VSV, the expression of VSV mRNA was detected by real-time quantitative PCR (RT-qPCR), and the expression of VSV-G was detected by western blotting. After transfecting poly (I:C) into PCYOX1 knockdown cells, the changes in mRNA levels of IFN-β, CXCL10, and ISG56 were detect by RT-qPCR, western blotting was performed to detect the changes in phosphorylation levels of interferon regulatory IRF3 and TBK1. Efficient knockdown and overexpression of PCYOX1 in BJ-5ta cells were successfully achieved. Compared with the negative control group, the copy number of VSV in PCYOX1 knockdown cells increased by 2.50-3.69 times (P<0.001) when infected with VSV-GFP, and the expression level of viral protein also significantly increased. After transfecting poly (I:C) into PCYOX1 knockdown cells, the phosphorylation level of IRF3, which is key transcription factor in innate type I interferon response, was significantly reduced, and the mRNA levels of IFN-β and interferon-stimulated genes CXCL10 and ISG56 were also significantly reduced. PCYOX1 gene knockdown enhances the infection and replication of VSV, and inhibits the activation of innate immunity mediated by type I interferon. It may serve as a key regulatory molecule in the resistance to RNA viruses.