C-Fos regulates hepatitis C virus propagation

Sang Min Kang, Seri Lim, Seung Jae Won, Ye Jin Shin, Yun Sook Lim, Byung Yoon Ahn, Soon B. Hwang

Research output: Contribution to journalArticlepeer-review

16 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)3236-3244
Number of pages9
JournalFEBS Letters
Issue number20
Publication statusPublished - 2011 Oct 20


  • Cellular factor
  • Hepatitis C virus
  • Pathogenesis
  • Propagation
  • c-Fos

ASJC Scopus subject areas

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology


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