Recombinant interferon-γ lentivirus co-infection inhibits adenovirus replication ex vivo.
Recombinant interferon-γ lentivirus co-infection inhibits adenovirus replication ex vivo.
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DOI：
10.1371/journal.pone.0042455
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发表时间：
2012
期刊：
影响因子：
3.7
通讯作者：
Li C
中科院分区：
文献类型：
--
作者：
Zhang L;Yin S;Tan W;Xiao D;Weng Y;Wang W;Li T;Shi J;Shuai L;Li H;Zhou J;Allain JP;Li C
探索了培养的慢病毒 (LV) 中重组干扰素-γ (IFNγ) 的产生，以抑制与 5 型腺病毒 (Ad5) 共感染的细胞中的靶病毒。在不同的细胞系中系统地评估了 CMV、EF1α 和泛素三种不同启动子在慢病毒内启动增强的绿色荧光蛋白（GFP）活性的能力，结果表明某些细胞系选择了最有利的启动子来驱动高水平的转基因表达。生成携带 CMV 启动子的重组 IFNγ 慢病毒 (LV-CMV-IFNγ)，与 LV-CMV-GFP 对照平行，用重组 GFP Ad5 的病毒替代物共感染 293A 细胞。两种慢病毒共感染的细胞观察到最佳形态条件，而单一腺病毒感染的细胞则出现明显的病理变化。 LV-CMV-IFNγ或LV-CMV-GFP共感染细胞培养物中的腺病毒载量显着低于腺病毒单独感染细胞中的病毒载量（P = 0.005–0.041），并且共感染细胞中腺病毒载量的减少分别为86%和61%。 LV-CMV-IFNγ共感染细胞的Ad5病毒载量显着低于LV-CMV-GFP共感染细胞（P = 0.032），这表明IFNγ而非GFP可以进一步增强重组慢病毒共感染细胞中Ad5复制的抑制作用。结果表明，LV-CMV-IFNγ共感染可显着抑制靶病毒复制，可能成为严重病毒性疾病替代治疗的潜在方法。
Recombinant interferon-γ (IFNγ) production in cultured lentivirus (LV) was explored for inhibition of target virus in cells co-infected with adenovirus type 5 (Ad5). The ability of three different promoters of CMV, EF1α and Ubiquitin initiating the enhanced green fluorescence protein (GFP) activities within lentiviruses was systematically assessed in various cell lines, which showed that certain cell lines selected the most favorable promoter driving a high level of transgenic expression. Recombinant IFNγ lentivirus carrying CMV promoter (LV-CMV-IFNγ) was generated to co-infect 293A cells with a viral surrogate of recombinant GFP Ad5 in parallel with LV-CMV-GFP control. The best morphologic conditions were observed from the two lentiviruses co-infected cells, while single adenovirus infected cells underwent clear pathologic changes. Viral load of adenoviruses from LV-CMV-IFNγ or LV-CMV-GFP co-infected cell cultures was significantly lower than that from adenovirus alone infected cells (P = 0.005–0.041), and the reduction of adenoviral load in the co-infected cells was 86% and 61%, respectively. Ad5 viral load from LV-CMV-IFNγ co-infected cells was significantly lower than that from LV-CMV-GFP co-infection (P = 0.032), which suggested that IFNγ rather than GFP could further enhance the inhibition of Ad5 replication in the recombinant lentivirus co-infected cells. The results suggest that LV-CMV-IFNγ co-infection could significantly inhibit the target virus replication and might be a potential approach for alternative therapy of severe viral diseases.
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