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Expression profiling of liver cell lines expressing entire or parts of hepatitis C virus open reading frame
Author(s) -
Aizaki Hideki,
Harada Takashi,
Otsuka Motoyuki,
Seki Naohiko,
Matsuda Mami,
Li Yue Wei,
Kawakami Hayato,
Matsuura Yoshiharu,
Miyamura Tatsuo,
Suzuki Tetsuro
Publication year - 2002
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840360620
Subject(s) - biology , open reading frame , hepatitis c virus , gene expression profiling , virology , gene , cell culture , gene expression , virus , liver cell , viral replication , microbiology and biotechnology , genetics , peptide sequence , medicine
Although hepatitis C virus (HCV) is a causative agent of liver diseases, its mechanism of pathogenesis is still unclear, mainly because of the lack of adequate cell culture systems to support HCV infection and replication. In this report, we describe development and characterization of human hepatoma cell lines constitutively expressing entire (Hep394) or parts (Hep352, Hep3294) of the HCV open reading frame (ORF). The viral and cellular proteolytic machinery involved in the viral precursor processing was consistently functional, and processed HCV proteins were synthesized in these established cell lines. By using a cDNA microarray analysis coupled with semiquantitative reverse‐transcription polymerase chain reaction (RT‐PCR), we identified 12 genes up‐regulated and 4 genes down‐regulated in Hep394 cells. With regard to genes related to cell growth regulation, we found up‐regulation of forkhead transcription factor FREAC‐1, poly (A) binding protein PABP2, and Ras suppressor Rsu‐1. Another category of changes in gene expression includes MHC antigens, which play an important role in the T‐cell‐mediated immune reaction in the liver. In conclusion, functional genomic approaches comparing expression among the different cell lines expressing parts of the HCV genome may promote our understanding of the molecular basis of pathogenicity of HCV infection. (H EPATOLOGY 2002;36:1431–1438).