Novel Evidence Suggests Hepatitis B Virus Surface Proteins Participate in Regulation of HBV Genome Replication
10.1007/s12250-011-3190-0
- Author:
Jian QIU
;
Bo QIN
;
Simon RAYNER
;
Chunchen WU
;
Rangjuan PEI
;
Song XU
;
Yun WANG
;
Xinwen CHEN
- Publication Type:Journal Article
- Keywords:
Hepatitis B virus(HBV);
HBsAg;
Truncated surface protein(TSPs);
Site-directed mutagenesis;
Alternative translation initiation
- From:
Virologica Sinica
2011;26(2):131-138
- CountryChina
- Language:Chinese
-
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 replicationdefective 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.
