Virologica Sinica

, Volume 26, Issue 2, pp 131–138

Novel evidence suggests Hepatitis B virus surface proteins participate in regulation of HBV genome replication

  • Jian Qiu
  • Bo Qin
  • Simon Rayner
  • Chun-chen Wu
  • Rong-juan Pei
  • Song Xu
  • Yun Wang
  • Xin-wen Chen
Article

DOI: 10.1007/s12250-011-3190-0

Cite this article as:
Qiu, J., Qin, B., Rayner, S. et al. Virol. Sin. (2011) 26: 131. doi:10.1007/s12250-011-3190-0

Abstract

Naturally occurring mutations in surface proteins of Hepatitis B virus (HBV) usually result in altered hepatitis B surface antigen (HBsAg) secretion efficiency. In the present study, we reported two conserved residues, M75 and M103 with respect to HBsAg, mutations of which not only attenuated HBsAg secretion (M75 only), but also suppressed HBV genome replication without compromising the overlapping p-gene product. We also found M75 and M103 can initiate truncated surface protein (TSPs) synthesis upon over-expression of full-length surface proteins, which may possibly contribute to HBV genome replication. However, attempts to rescue replication-defective HBV mutant by co-expression of TSPs initiated from M75 or M103 were unsuccessful, which indicated surface proteins rather than the putative TSPs were involved in regulation of HBV genome replication.

Key words

Hepatitis B virus (HBV) HBsAg Truncated surface protein (TSPs) Site-directed mutagenesis Alternative translation initiation 

Copyright information

© Wuhan Institute of Virology, CAS and Springer-Verlag Berlin Heidelberg 2011

Authors and Affiliations

  • Jian Qiu
    • 1
    • 2
  • Bo Qin
    • 1
    • 2
  • Simon Rayner
    • 1
  • Chun-chen Wu
    • 1
  • Rong-juan Pei
    • 1
  • Song Xu
    • 1
  • Yun Wang
    • 1
  • Xin-wen Chen
    • 1
  1. 1.State Key Laboratory of Virology, Wuhan Institute of VirologyChinese Academy of SciencesWuhanChina
  2. 2.Graduate University of the Chinese Academy of SciencesBeijingChina

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