EPSTI1 is involved in IL-28A-mediated inhibition of HCV Infection

Xianghe Meng, Darong Yang, Rong Yu, Haizhen Zhu

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

It has been reported that IFN-λs inhibit HCV replication in vitro. But the mechanisms of how IL-28A conducts antiviral activity and the functions of IL-28A-induced ISGs (IFN-stimulated genes) are not fully understood. In this study, we found that IL-28A has the antiviral effect on HCV life cycle including viral replication, assembly, and release. IL-28A and IFN- synergistically inhibit virus replication. EPSTI1 (epithelial-stromal interaction 1), one of IL-28A-induced ISGs, plays a vital role in IL-28A-mediated antiviral activity. Furthermore, forced expression of EPSTI1 effectively inhibits HCV replication in the absence of interferon treatment, and knockdown of EPSTI1 contributes to viral enhancement. EPSTI1 can activate PKR promoter and induce several PKR-dependent genes, including IFN-β, IFIT1, OAS1, and RNase L, which is responsible for EPSTI1-mediated antiviral activity.

Original languageEnglish (US)
Article number716315
JournalMediators of Inflammation
Volume2015
DOIs
StatePublished - Jan 1 2015

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Antiviral Agents
Infection
Genes
Virus Assembly
Virus Replication
Life Cycle Stages
Interleukin-1
Interferons

All Science Journal Classification (ASJC) codes

  • Immunology
  • Cell Biology

Cite this

EPSTI1 is involved in IL-28A-mediated inhibition of HCV Infection. / Meng, Xianghe; Yang, Darong; Yu, Rong; Zhu, Haizhen.

In: Mediators of Inflammation, Vol. 2015, 716315, 01.01.2015.

Research output: Contribution to journalArticle

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abstract = "It has been reported that IFN-λs inhibit HCV replication in vitro. But the mechanisms of how IL-28A conducts antiviral activity and the functions of IL-28A-induced ISGs (IFN-stimulated genes) are not fully understood. In this study, we found that IL-28A has the antiviral effect on HCV life cycle including viral replication, assembly, and release. IL-28A and IFN- synergistically inhibit virus replication. EPSTI1 (epithelial-stromal interaction 1), one of IL-28A-induced ISGs, plays a vital role in IL-28A-mediated antiviral activity. Furthermore, forced expression of EPSTI1 effectively inhibits HCV replication in the absence of interferon treatment, and knockdown of EPSTI1 contributes to viral enhancement. EPSTI1 can activate PKR promoter and induce several PKR-dependent genes, including IFN-β, IFIT1, OAS1, and RNase L, which is responsible for EPSTI1-mediated antiviral activity.",
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