论文部分内容阅读
目的:探讨CpG寡脱氧核苷酸链(CpG ODN)体外对EB病毒(EBV)复制的抑制作用。方法:CpG ODN体外预处理人外周血单个核细胞(PBMC)后感染EBV,用荧光定量PCR和ELISA分别检测培养后PBMC中EBV拷贝数和培养上清液中γ干扰素(IFN-γ)的水平,了解不同剂量、不同时间CpG ODN预处理PBMC中EBV复制和PBMC产生IFN-γ之间的关系。结果:(1)不同浓度CpG ODN预处理组的EBV拷贝数均低于未处理组(P<0.05),其中10mg/LCpG ODN预处理组EBV拷贝数最低,为(3.85±0.37)×108基因拷贝/L;(2)CpG ODN预处理48h组的EBV拷贝数(11.32±0.83)×108基因拷贝/L低于其余各预处理时间组的EBV拷贝数(P<0.05);(3)不同浓度CpG ODN预处理组培养上清液中的IFN-γ均高于PBMC组和PBMC+EBV组(P<0.05),其中10mg/LCpG ODN处理组IFN-γ量最高(66.27±6.29)ng/L;(4)CpG ODN预处理48h的PBMC+CpG ODN+EBV组培养上清液中IFN-γ(51.74±4.09)ng/L高于其余各预处理时间组和PBMC组及PBMC+EBV组(P<0.05)。结论:CpGODN作为一种新型的免疫调节剂,在体外能有效抑制EBV复制,其作用机制可能与诱导PBMC产生IFN-γ有关。
Objective: To investigate the inhibitory effect of CpG ODN on the replication of Epstein-Barr virus (EBV) in vitro. Methods: EBV was infected with CpG ODN pretreated with human peripheral blood mononuclear cells (PBMCs) in vitro and the EBV copy number and IFN-γ in the supernatant were detected by fluorescence quantitative PCR and ELISA respectively Level, to understand the different doses, different time CpG ODN pretreatment EBV replication in PBMC and PBMC to produce IFN-γ relationship. Results: (1) The EBV copy number of the pretreatment group with different concentrations of CpG ODN was lower than that of the untreated group (P <0.05). The EBV copy number of the 10mg / LCpG ODN pretreatment group was the lowest (3.85 ± 0.37) × 108 (2) The EBV copy number (11.32 ± 0.83) × 108 gene copies / L in the 48h group after CpG ODN pretreatment was lower than those in other pretreatment time groups (P <0.05); (3) The IFN-γ in supernatant of CpG ODN pretreatment group was higher than that in PBMC group and PBMC + EBV group (P <0.05), and the highest IFN-γ level in ODN-treated group was (66.27 ± 6.29) ng / L; (4) IFN-γ in supernatant of PBMC + CpG ODN + EBV pretreated with CpG ODN 48h was significantly higher than that of other preconditioning groups and PBMC + PBMC + EBV group (51.74 ± 4.09) ng / L (P <0.05). Conclusion: As a novel immunomodulatory agent, CpGODN can effectively inhibit EBV replication in vitro. Its mechanism may be related to the induction of IFN-γ production by PBMCs.