Interactions between Heparin cofactor II and hepatitis C virus

• Main Authors: Yu-Lin Huang, 黃玉玲
• Other Authors: Shih-Yen Lo
• Format: Others
• Language: zh-TW
• Published: 2012
• Online Access: http://ndltd.ncl.edu.tw/handle/58929794159432531510

碩士 === 慈濟大學 === 醫學檢驗生物技術學系醫學生物技術碩士班 === 100 === Infection with hepatitis C virus (HCV) could cause chronic infection, liver cirrhosis, and even hepatocellular carcinoma (HCC) and more than 170 million people were infected around the world. At present, neither an effective treatment to chronic HCV infection nor a vaccine to prevent HCV infection is available. Identification of host factors involved in viral replication is critical for understanding the molecular mechanism of virus replication. Identification of host factors involved in viral replication also facilitates the development of anti-viral agents. Genes differentially expressed (over-expressed or down-regulated) in HCV replicon cells with or without HCV sub-genomic replicon (RE* cell) were identified by dd-RT-PCR . Genes over-expressed in HCV replicon cells could be the factors facilitating HCV replication while down-regulated genes could be the factors repressing the HCV replication. Heparin cofactor II (HCII) identified was down-regulated in HCV replicon cells. Our results showed HCII could indeed inhibit HCV replication. HCII represses the HCV replication possibly through interacting with HCV NS3 protein. The binding domains of HCII and HCV NS3 protein were also determined by yeast two-hybrid system. Furthermore, different HCII mutants (1~212、 20~212、20~499、213~499) were transfected into HCV replicon cells. Our results indicated that except the 20~212, all HCII mutants can repress the HCV replication. On the other hand, we have tried to find out which treatment or HCV gene product could reduce the HCII expression. However, no conclusive results were obtained. Therefore, the mechanism how the HCV down-regulated HCII gene expression needs further investigation.