| セッション情報 |
Hepatitis C i)Hepatitis C and HCC(II)
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| タイトル |
IF4c-6 Host Factors Determining the Efficacy of Hepatitis C Treatment in Japan
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| 演者 |
Yasuhito Tanaka（Department of Virology & Liver UnitNagoya City University Graduate School of Medical SciencesJapan） |
| 共同演者 |
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| 抄録 |
The current standard of care （SOC） is combination treatment with pegylated interferon and ribavirin（PEG－IFN／RBV）but this costly and poorly tolerated treatment achieves sustained virological response inonly 50 O／o of patients． Several large genome－wide association studies （GWAS） have identified single nucleo－tide polymorphisms （SNPs） linked to llL28B gene （IFN－X3） that are associated with the spontaneous reso－lution and successful treatment of HCV infection． ClinicallyIL28B SNPs can predict the virological re－sponse by SOC as well as recently approved SOC pltts the first direct－acting antiviral agents （DAAs） in－cluding telaprevir．and boceprevir． Japanese studies showeld that the combination of皿28－B SNPs andamino acid substitutions at positions 70 of the H／CV core protein improved the prediction of SVR by SOCplus telaprevir． Howeverit is not yet clear how IFN－X3 SNPs linked to the risk allele identifiTed in theGWAS affect immune function or exert specific antivira 1 effects in H：CV－infected patients． As for the cur－rently known biology of IFN－Xs1） two studies found that the favorable SNP is associated with increasedlevels of IFN－X3 in PBMCs． 2） Myeloid dendritic ￠ell 2 （mDC2） and macrophages are the main producersof IFN－X stimulated by viruses and viral or bacterial mimics． 3） IF’N－X has a restricted receptor distributionand therefore restricted targets． 4） Up－regulated hepatic ISGs pretreatment are associated with the IFN－X3 risk allele and with poor treatment outcome． These data suggest that the effect of IFN－X3 on HCV clini－cal outcome is肱ely to be a complex interaction between IFN一αHCV itselfISGs and immunomodulation． |
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