title: Novel evidence suggests Hepatitis B virus surface proteins participate in regulation of HBV genome replication.
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.
authors.affiliation: Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071, China.
authors.forename: Jian
authors.initials: J
authors.lastname: Qiu
authors.forename: Bo
authors.initials: B
authors.lastname: Qin
authors.forename: Simon
authors.initials: S
authors.lastname: Rayner
authors.forename: Chun-chen
authors.initials: CC
authors.lastname: Wu
authors.forename: Rong-juan
authors.initials: RJ
authors.lastname: Pei
authors.forename: Song
authors.initials: S
authors.lastname: Xu
authors.forename: Yun
authors.initials: Y
authors.lastname: Wang
authors.forename: Xin-wen
authors.initials: XW
authors.lastname: Chen
mesh_terms: D002460:Cell Line; D006509:Hepatitis B / Q000821:virology; D006514:Hepatitis B Surface Antigens / Q000235:genetics / Q000378:metabolism*; D006515:Hepatitis B virus / Q000235:genetics / Q000502:physiology*; D006801:Humans; D009154:Mutation; D014779:Virus Replication
chemical_list: D006514:Hepatitis B Surface Antigens