Abstract
Objective To investigate the effect of exogenous interferon (IFN) -β on the expression of endogenous type I IFN and the localization of interferon regulatory factor (IRF) 7 in human oligodendrocyte (OL) and Borna disease virus (BDV) persistently infected OL cells (OL/BDV). Methods The expression of type I IFN mRNA was detected by quantitative real-time PCR (qPCR) after OL cells and OL/BDV cells were treated with exogenous IFN-β for 0, 0.5, 2, 4, 8 h and 24 h. According to whether the exogenous IFN-β was added to the cell culture, cells were divided into exogenous IFN-β unstimulated and stimulated cells.The localization of IRF7 was observed after OL cells and OL/BDV cells were transfected with IRF7-EGFP plasmids and stimulated with exogenous IFN-β for 4 h. Results The expression of IFN-α mRNA was increased when OL cells were stimulated by exogenous IFN-β for 2, 4 h, and 24 h (P values were 0.008, 0.0001, 0.004, respectively). The expression of IFN-β mRNA was increased when cells were treated for 0.5, 4, 8, 24 h(P values were 0.0004, 0.0002, 0.011, 0.012 respectively). The most significant increase for IFN-α and IFN-β mRNA were all at 4 h after treatment.The expression of IFN-α mRNA in OL/BDV cells which were treated with the same stimulation as for OL cells, increased at 4 h and 24 h(P values were 0.0004, 0.022 respectively). The expression of IFN-β mRNA increased only when treated for 4 h (P=0.002). Meanwhile, IRF7 green fluorescent protein translocated into the nucleus in OL and OL/BDV cells treated with exogenous IFN-β stimulated for 4 h. Conclusions Exogenous IFN-β induces the expression of endogenous type I IFN in OL and OL/BDV cells.Moreover, endogenous IFN-β participates in releasing the suppression of BDV toward type I IFN, and promotes the activation of IRF7. Key words: Exogenous interferon -β; Human oligodendrocyte; Borna disease virus persistently infected human oligodendrocyte; Endogenous type I interferon
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
