| Literature DB >> 17563922 |
Kohji Moriishi1, Yoshiharu Matsuura.
Abstract
Hepatitis C virus (HCV) is the major causative agent of blood-borne hepatitis. The majority of HCV-infected individuals develop chronic hepatitis, which eventually progresses to liver cirrhosis, and hepatocellular carcinoma. Although the precise mechanisms of entry, replication, assembly, egress and pathogenesis of HCV are largely unknown, information about viral receptor candidates has accumulated by the development of pseudotype viruses and an in vitro replication system of the HCV JFH1 strain. Furthermore, the autonomous RNA replication system based on the artificial viral genome revealed that HCV replicates in the intracellular replication complex composed of viral and host proteins. Recently, an immunosuppress ant, cyclosporin A and inhibitors for sphingolipid synthesis and chaperon were reported to inhibit the replication of HCV by counteracting the interplay between host and viral proteins. This review considers the current knowledge of the host proteins that participate in HCV replication and the possibility of developing novel therapeutics intervention for chronic hepatitis C.Entities:
Mesh:
Substances:
Year: 2007 PMID: 17563922 DOI: 10.1002/rmv.542
Source DB: PubMed Journal: Rev Med Virol ISSN: 1052-9276 Impact factor: 6.989