Replication of the hepatitis B virus requires a calcium-dependent HBx-induced G1 phase arrest of hepatocytes.
Replication of the hepatitis B virus requires a calcium-dependent HBx-induced G1 phase arrest of hepatocytes.
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DOI：
10.1016/j.virol.2010.07.042
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发表时间：
2010-11-10
期刊：
影响因子：
3.7
通讯作者：
Bouchard MJ
中科院分区：
文献类型：
--
作者：
Gearhart TL;Bouchard MJ
慢性HBV感染导致肝细胞癌（HCC）。HBV HBx蛋白的活性调节HBV复制，并可能有助于HCC的发展。我们以前报道，HBx导致原代大鼠肝细胞退出G0，但停滞在G1期的细胞周期，进入G1刺激HBV复制。我们现在报告，线粒体通透性转换孔的活性是HBx调节细胞周期蛋白和HBV复制所需的原代大鼠肝细胞，从G0到G1的进展刺激HBV聚合酶活性，HBV复制是由HBx诱导的G1停滞促进。HBx对HBV复制的刺激与核糖核苷酸还原酶R2亚基的升高有关。我们的研究表明，HBx使用肝细胞依赖性钙信号，使肝细胞退出G0，但停滞在G1，这种HBx的活动改变了细胞环境，刺激HBV复制。
Chronic HBV infections cause hepatocellular carcinoma (HCC). Activities of the HBV HBx protein regulate HBV replication and may contribute to the development of HCC. We previously reported that HBx causes primary rat hepatocytes to exit G0 but stall in G1 phase of the cell cycle; entry into G1 stimulated HBV replication. We now report that the activity of the mitochondria permeability transition pore is required for HBx regulation of cell cycle proteins and HBV replication in primary rat hepatocytes, that progression from G0 to G1 stimulates HBV polymerase activity, and that HBV replication is facilitated by the HBx-induced G1 arrest. HBx stimulation of HBV replication was linked to elevation of the R2 subunit of ribonucleotide reductase. Our studies suggest that HBx uses mitochondrial-dependent calcium signaling to cause hepatocytes to exit G0 but stall in G1 and that this HBx activity alters the cellular environment and stimulates HBV replication.
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