Type I and type II interferon responses in two human liver cell lines (Huh-7 and HuH6).
Type I and type II interferon responses in two human liver cell lines (Huh-7 and HuH6).
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DOI：
10.1016/j.gdata.2015.12.017
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发表时间：
2016-03
期刊：
影响因子：
--
通讯作者：
Binder M
中科院分区：
文献类型：
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作者：
Grünvogel O;Esser-Nobis K;Windisch MP;Frese M;Trippler M;Bartenschlager R;Lohmann V;Binder M
大多数调查丙型肝炎病毒 (HCV) 生物学的研究都使用人肝癌细胞系 Huh-7 或其亚克隆，因为这些是最容易感染和复制 HCV 的细胞系。其他细胞系也支持 HCV 复制，最著名的是人肝母细胞瘤细胞系 HuH6。细胞培养中的 HCV 复制通常对干扰素 (IFN) 高度敏感，并且 IFN 介导的病毒复制抑制的差异可能反映了不同宿主细胞固有的 IFN 诱导的抗病毒反应的变化。例如，在 Huh-7 细胞中，HCV 复制对 IFN-γ 处理高度敏感，但在 HuH6 细胞中则不然。在本研究中，我们使用基于微阵列的基因表达谱来比较 Huh-7 和 HuH6 细胞对 IFN-α 和 IFN-γ 刺激的反应。此外，我们还确定了 HuH6 细胞中 HCV 复制的抵抗是否与 IFN 调节基因表达谱的差异有关。尽管两种细胞系对干扰素的反应都导致基因表达发生快速变化，从而证明了功能性 I 型和 II 型信号通路，但仍观察到许多基因存在差异。原始和标准化表达数据已以登录号 GSE68927 保存在 GEO 中。
Most studies investigating the biology of Hepatitis C virus (HCV) have used the human hepatoma cell line Huh-7 or subclones thereof, as these are the most permissive cell lines for HCV infection and replication. Other cell lines also support replication of HCV, most notably the human hepatoblastoma cell line HuH6. HCV replication in cell culture is generally highly sensitive to interferons (IFNs) and differences in the IFN-mediated inhibition of virus replication may reflect alterations in the IFN-induced antiviral response inherent to different host cells. For example, HCV replication is highly sensitive to IFN-γ treatment in Huh-7, but not in HuH6 cells. In this study, we used microarray-based gene expression profiling to compare the response of Huh-7 and HuH6 cells to stimulation with IFN-α and IFN-γ. Furthermore, we determined whether the resistance of HCV replication in HuH6 cells can be linked to differences in the expression profile of IFN-regulated genes. Although both cells lines responded to IFNs with rapid changes in gene expression, thereby demonstrating functional type I and type II signaling pathways, differences were observed for a number of genes. Raw and normalized expression data have been deposited in GEO under accession number GSE68927.