13:40 - 15:10
Room: ANA Crowne Plaza “Ohtori” Room C
Workshop Session
Chair/s:
Koji Yasutomo, Warren Leonard
Virus-induced IFN-λ4 potently blocks IFN-α signaling by ISG15/USP18 in HCV infection
Seon-Hui Hong
Korea Advanced Institute of Science and Technology, Daejeon, Korea, Republic of (South)

Introduction & Aims : IFN-l4 is a newly identified type III IFN and the dinucleotide polymorphism of IFN-l4 has been a genetic marker strongly associated with response to IFN-α based therapy in hepatitis C virus (HCV)-infected patients. The IFNL4-TT genotype does not produce IFN-l4 due to a premature stop codon, while the IFNL4-DG genotype is a frameshift variant that produces functional IFN-l4. It is reported that HCV-infected patients with the IFNL4-TT genotype show favorable response to IFN-α based therapy whereas patients with the IFNL4-DG show poor response to IFN-α based therapy. However, the underlying mechanism of these genotype-phenotype correlation is not fully investigated. In our previous study, we demonstrated that prolonged exposure to IFNs results in unresponsiveness to IFN-α by ISG15 upregulation and USP18 stabilization. In this study, we investigated the induction of IFN-l4 by HCV infection and the biological effects of IFN-l4 in relation to IFN-α responsiveness.

Methods : Huh7 cells were transfected with IFNL4 encoding plasmid or treated with recombinant human IFN-l4. Primary human hepatocytes (PHHs) with IFNL4-DG allele were infected with JFH1 HCVcc at high titer to examine the effects of IFN-l4 on IFN-α responsiveness

Results : HCV infection induced IFN-l4 at mRNA and protein level in PHHs with IFNL4-DG allele. HCV-infected PHHs showed attenuated response to exogenous IFN-α. IFN-l4 treatment or IFNL4 encoding plasmid transfection caused sustained upregulation of ISG15 and USP18 in Huh7 cells, resulting in IFN-α unresponsiveness. The ISG15/USP18 mediated IFN-α unresponsiveness was confirmed by transfection of siRNA targeting ISG15 or USP18. Direct-acting antivirals (DAAs) treatment to HCV-infected PHHs decreased the induction of IFN-λs including IFN-λ4 and restored the IFN-α responsiveness.

Conclusion : Our data demonstrate that IFN-l4 induced by HCV infection confers unresponsiveness to IFN-α by upregulation of ISG15 and USP18. HCV-infected hepatocytes restore IFN-α responsiveness after DAA treatment.


Reference:
Mo-WS5-7
Session:
Workshop 5, “Genetic disorders in cytokines and inflammation”
Presenter/s:
Seon-Hui Hong
Presentation type:
Oral Presentation
Room:
ANA Crowne Plaza “Ohtori” Room C
Chair/s:
Koji Yasutomo, Warren Leonard
Date:
Monday, 30 October 2017
Time:
15:00 - 15:10
Session times:
13:40 - 15:10