Synergetic transactivating effect of HCV core and HBV X proteins on SV40 early promoter/enhancer.
- Author:
Yan LIU
1
;
Jun CHENG
;
De-zhi SHAO
;
Lin WANG
;
Yan-wei ZHONG
;
Jing DONG
;
Ke LI
;
Li LI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Carcinoma, Hepatocellular; virology; Enhancer Elements, Genetic; Hepacivirus; genetics; Hepatitis C Antigens; genetics; Humans; Liver Neoplasms; virology; Promoter Regions, Genetic; drug effects; Simian virus 40; genetics; Trans-Activators; genetics; Transcriptional Activation; Viral Core Proteins; genetics; beta-Galactosidase; biosynthesis; genetics
- From: Chinese Journal of Experimental and Clinical Virology 2003;17(1):70-72
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUNDTo investigate the synergetic transactivating effects of HCV core and HBV X proteins.
METHODSHCV core and HBV X protein-expressing plasmids were constructed with the vector pcDNA3.1(-). The plasmids were transfected into HepG2 cells and cotransfected Hep2 cells with reporter plasmid Psv-lacZ by lipofectamine plus reagents. The virus proteins produced in transient expression system were detected at the transcription and translation levels. The activity of b-galactosidase was detected, which reflected the transactivating function of the proteins.
RESULTSThe expression of plasmids were detected in soluble protein cell extracts of transiently transfected HepG2 cells. HCV core protein activated the b-galactosidase expression at a value 4.9 times higher than the control, while HBV X protein activated at a value 3.5 times. It arrived at 9 times transfected with the plasmids simultaneously. The activating effect increased in relation to the amount of plasmids.
CONCLUSIONSThe results suggested that the two kinds of virus proteins have transactivating effect on SV40 early promoter/enhancer, and they acted synergistically. These contribute to explain the mechanisms of liver injury or tumorigenesis induced by HCV or/and HBV infection.