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c‐Fos regulates hepatitis C virus propagation
Author(s) -
Kang Sang-Min,
Lim Seri,
Won Seung-Jae,
Shin Ye-Jin,
Lim Yun-Sook,
Ahn Byung-Yoon,
Hwang Soon B.
Publication year - 2011
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2011.08.041
Subject(s) - hepatitis c virus , gene silencing , virology , c fos , rna interference , small interfering rna , downregulation and upregulation , pathogenesis , biology , cell culture , transfection , microbiology and biotechnology , luciferase , virus , rna , gene expression , immunology , gene , biochemistry , genetics
Hepatitis C virus (HCV) RNA replication requires cellular factors as well as viral non‐structural proteins (NS protein). Using small interfering RNA (siRNA) library screening, we previously identified c‐Fos as a host factor involved in HCV propagation. In the present study, we demonstrated that silencing of c‐Fos expression resulted in decrease of HCV propagation in cell culture grown HCV (HCVcc)‐infected cells; whereas overexpression of c‐Fos significantly increased HCV propagation. We further confirmed the positive role of c‐Fos in HCV propagation by both HCV‐luciferase reporter assay and immunofluorescence analysis. We showed that c‐Fos level was upregulated by HCV infection. Furthermore, phorbol 12‐myristate 13‐acetate (PMA)‐induced c‐Fos level was synergistically increased by HCV infection. These data suggest that c‐Fos acts as a positive regulator of HCV propagation and may contribute to HCV‐associated pathogenesis.