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http://purl.uniprot.org/citations/24929144http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/24929144http://www.w3.org/2000/01/rdf-schema#comment"Natural killer cells play a key role in the immune control of viral infections. Killer immunoglobulin-like receptors (KIRs) regulate natural killer cell activation and inhibition through the recognition of their cognate HLA class I ligands. We assessed the predictive factors of a sustained virological response (SVR) in 200 Japanese patients with chronic genotype 1b hepatitis C who were treated with telaprevir (TVR), pegylated-interferon-α2b (PEG-IFN), and ribavirin (RBV) triple therapy (92 patients) or PEG-IFN/RBV therapy alone (108 patients). Sixteen KIR genotypes, HLA-A, -B and -C ligands, and an interleukin (IL) 28B polymorphism (rs8099917) were analyzed. We observed that triple therapy, white blood cell count, hemoglobin value, hepatitis C viral load, a rapid virological response (RVR), IL28B TT genotype, and KIR3DL1-HLA-Bw4 genotype were associated with an SVR. In multivariate regression analysis, we identified an RVR (P < 0.000001; odds ratio [OR] = 20.95), the IL28B TT genotype (P = 0.00014; OR = 5.53), and KIR3DL1-HLA-Bw4 (P = 0.004, OR = 3.42) as significant independent predictive factors of an SVR. In conclusion, IL28B and KIR3DL1/HLA-Bw4 are independent predictors of an SVR in Japanese patients infected with genotype 1b HCV receiving TVR/PEG-IFN/RBV or PEG-IFN/RBV therapy."xsd:string
http://purl.uniprot.org/citations/24929144http://purl.org/dc/terms/identifier"doi:10.1016/j.humimm.2014.06.003"xsd:string
http://purl.uniprot.org/citations/24929144http://purl.uniprot.org/core/author"Kobayashi M."xsd:string
http://purl.uniprot.org/citations/24929144http://purl.uniprot.org/core/author"Kimura T."xsd:string
http://purl.uniprot.org/citations/24929144http://purl.uniprot.org/core/author"Mori H."xsd:string
http://purl.uniprot.org/citations/24929144http://purl.uniprot.org/core/author"Maruyama A."xsd:string
http://purl.uniprot.org/citations/24929144http://purl.uniprot.org/core/author"Umemura T."xsd:string
http://purl.uniprot.org/citations/24929144http://purl.uniprot.org/core/author"Shibata S."xsd:string
http://purl.uniprot.org/citations/24929144http://purl.uniprot.org/core/author"Tanaka E."xsd:string
http://purl.uniprot.org/citations/24929144http://purl.uniprot.org/core/author"Katsuyama Y."xsd:string
http://purl.uniprot.org/citations/24929144http://purl.uniprot.org/core/author"Nozawa Y."xsd:string
http://purl.uniprot.org/citations/24929144http://purl.uniprot.org/core/author"Matsumoto A."xsd:string
http://purl.uniprot.org/citations/24929144http://purl.uniprot.org/core/author"Wada S."xsd:string
http://purl.uniprot.org/citations/24929144http://purl.uniprot.org/core/author"Ota M."xsd:string
http://purl.uniprot.org/citations/24929144http://purl.uniprot.org/core/author"Yoshizawa K."xsd:string
http://purl.uniprot.org/citations/24929144http://purl.uniprot.org/core/author"Morita S."xsd:string
http://purl.uniprot.org/citations/24929144http://purl.uniprot.org/core/author"Komatsu M."xsd:string
http://purl.uniprot.org/citations/24929144http://purl.uniprot.org/core/author"Kiyosawa K."xsd:string
http://purl.uniprot.org/citations/24929144http://purl.uniprot.org/core/author"Takamatsu M."xsd:string
http://purl.uniprot.org/citations/24929144http://purl.uniprot.org/core/author"Joshita S."xsd:string
http://purl.uniprot.org/citations/24929144http://purl.uniprot.org/core/author"Kamijo A."xsd:string
http://purl.uniprot.org/citations/24929144http://purl.uniprot.org/core/date"2014"xsd:gYear
http://purl.uniprot.org/citations/24929144http://purl.uniprot.org/core/name"Hum Immunol"xsd:string
http://purl.uniprot.org/citations/24929144http://purl.uniprot.org/core/pages"822-826"xsd:string