Epigenetic silencing of antiviral genes renders clones of Huh-7 cells permissive for hepatitis C virus replication

Qiuyue Chen, Bray Denard, Hua Huang, Jin Ye

Research output: Contribution to journalArticle

15 Scopus citations

Abstract

Hepatitis C virus (HCV) does not replicate efficiently in wild-type human hepatoma Huh-7 cells, but it replicates robustly in certain subclones of Huh-7 cells. Previously, we demonstrated that silencing of cyclic AMP (cAMP) response element binding protein 3-like 1 (CREB3L1), a cellular transcription factor that inhibits HCV replication, allows HCV to replicate in HRP1 cells, a subclone of Huh-7 cells permissive for HCV replication. Here we show that silencing of myxovirus resistant 1 (MX1), a known interferon-induced antiviral gene, is responsible for HRP4 cells, another subclone of Huh-7 cells, being permissive for HCV replication. Both CREB3L1 and MX1 are epigenetically silenced through DNA methylation in HRP1 and HRP4 cells, respectively. We further demonstrate that Huh-7 cells exist as a mixed population of cells with distinct patterns of gene methylation and HCV replicates in subpopulations of Huh-7 cells that have antiviral genes epigenetically silenced by DNA hypermethylation. Our results demonstrate that understanding the mechanism through which subclones of Huh-7 cells become permissive for HCV replication is crucial for studying their interaction with HCV.

Original languageEnglish (US)
Pages (from-to)659-665
Number of pages7
JournalJournal of virology
Volume87
Issue number1
DOIs
StatePublished - Jan 1 2013

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Insect Science
  • Virology

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