Hepatitis B virus (HBV) genome P-encoded protein-HBV DNA polymerase (Pol) has long been known as a reverse transcriptase during the HBV replication. In this study, we aimed at investigating the impact of HBV Pol on host cellular processes, mainly apoptosis, and the underlying mechanisms. We showed a marked reduction in apoptotic rates in the HBV Pol-expressed HepG2 cells compared to controls. Moreover, a series of assays-i.e. yeast two-hybrid, GST pull-down, co-immunoprecipitation, and confocal laser scanning microscopy-identified the host factor eEF1A2 to be associated with HBV Pol. Furthermore, knockdown of the eEF1A2 gene by siRNA abrogated the HBV Pol-mediated anti-apoptotic effect with apoptosis induced by endoplasmatic reticulum (ER) stress inducer thapsigargin (TG), thus suggesting that the host factor eEF1A2 is essential for HBV Pol's anti-apoptosis properties. Our findings have revealed a novel role for HBV Pol in its modulation of apoptosis through integrating with eEF1A2.

中文翻译：

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乙型肝炎病毒 DNA 聚合酶通过与肝癌细胞中的延伸因子 1-alpha2 相互作用显示出抗细胞凋亡作用。

乙型肝炎病毒 (HBV) 基因组 P 编码蛋白-HBV DNA 聚合酶 (Pol) 长期以来一直被认为是 HBV 复制过程中的逆转录酶。在这项研究中，我们旨在研究 HBV Pol 对宿主细胞过程（主要是细胞凋亡）的影响及其潜在机制。与对照组相比，我们发现表达 HBV Pol 的 HepG2 细胞的凋亡率显着降低。此外，一系列检测——即酵母双杂交、GST pull-down、免疫共沉淀和共聚焦激光扫描显微镜——确定了与 HBV Pol 相关的宿主因子 eEF1A2。此外，通过 siRNA 敲低 eEF1A2 基因消除了 HBV Pol 介导的抗细胞凋亡作用，内质网 (ER) 应激诱导剂毒胡萝卜素 (TG) 诱导细胞凋亡，因此表明宿主因子 eEF1A2 对 HBV Pol' 至关重要 s 抗凋亡特性。我们的研究结果揭示了 HBV Pol 通过与 eEF1A2 整合调节细胞凋亡的新作用。