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Hepatitis B Virus DNA Polymerase Displays an Anti-Apoptotic Effect by Interacting with Elongation Factor-1 Alpha-2 in Hepatoma Cells

  • Niu, Xianli (Department of Biochemistry and Molecular Biology, Zunyi Medical University) ;
  • Nong, Shirong (Key Laboratory of Genetic Engineering and Medicine, Key Laboratory of Viral Biology, Jinan University) ;
  • Gong, Junyuan (Key Laboratory of Genetic Engineering and Medicine, Key Laboratory of Viral Biology, Jinan University) ;
  • Zhang, Xin (Key Laboratory of Genetic Engineering and Medicine, Key Laboratory of Viral Biology, Jinan University) ;
  • Tang, Hui (Key Laboratory of Genetic Engineering and Medicine, Key Laboratory of Viral Biology, Jinan University) ;
  • Zhou, Tianhong (Key Laboratory of Genetic Engineering and Medicine, Key Laboratory of Viral Biology, Jinan University) ;
  • Li, Wei (Key Laboratory of Genetic Engineering and Medicine, Key Laboratory of Viral Biology, Jinan University)
  • Received : 2020.02.20
  • Accepted : 2020.10.21
  • Published : 2021.01.28

Abstract

Hepatitis B virus (HBV) genome P-encoded protein HBV DNA polymerase (Pol) has long been known as a reverse transcriptase during HBV replication. In this study, we investigated 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 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.

Keywords

References

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