Study of the effect of hepatitis C virus core protein on interferon-induced antiviral genes expression and its mechanisms.
- Author:
Yan-Zi CHANG
1
;
Yan-Chang LEI
;
You-Hua HAO
;
Shan-Shan CHEN
;
Wen WU
;
Dong-Liang YANG
;
Meng-Ji LU
Author Information
1. Department of Microbiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
- Publication Type:Journal Article
- MeSH:
2',5'-Oligoadenylate Synthetase;
genetics;
metabolism;
Carcinoma, Hepatocellular;
pathology;
Down-Regulation;
Hepacivirus;
genetics;
metabolism;
Humans;
Interferon-Stimulated Gene Factor 3;
genetics;
metabolism;
Interferon-alpha;
genetics;
immunology;
Liver Neoplasms;
pathology;
Protein Kinases;
genetics;
metabolism;
STAT1 Transcription Factor;
genetics;
metabolism;
STAT2 Transcription Factor;
genetics;
metabolism;
Transcription, Genetic;
Transfection;
Tumor Cells, Cultured;
Viral Core Proteins;
genetics;
metabolism;
physiology
- From:
Chinese Journal of Biotechnology
2007;23(6):1000-1004
- CountryChina
- Language:Chinese
-
Abstract:
To study the effect of HCV core protein on the interferon-induced antiviral genes expression and its mechanisms. Methods HepG2 cells were transiently transfected with HCV core protein expression plasmid and the blank plasmid respectively. RT-PCR was used to analyze the effect of HCV core protein on PKR and 2'-5'OAS expression. The effect of HCV core protein on ISRE-medicated gene expression was detected by luciferase activity assay. Western-blot assay was performed to observe the change of mRNA and protein levels of SOCS3, STAT1 and p-STAT1 following HCV core expression. In the presence of HCV core protein, the transcription of PKR and 2'-5' OAS are down-regulated. ISRE-medicated reporter gene expression and STAT1 phosphorylation were inhibited. The transcription and expression of SOCS3 were induced compared with blank plasmid-transfected group. In HepG2 cells, HCV core protein can down-regulate the expression of some interferon-induced antiviral genes, which involves the induction of SOCS3 and the inhibition of STAT1 phosphorylation.
