http://purl.uniprot.org/citations/16894313 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/16894313 | http://www.w3.org/2000/01/rdf-schema#comment | "ObjectiveInterferon-alpha (IFN-alpha), an important mediator for the host's innate antiviral defense system, has been approved for the treatment of persistent viral infections. We investigated whether two functional polymorphisms in genes involved in IFN-alpha signaling and effector functions are associated with the natural outcome of hepatitis C virus (HCV) infection and the responsiveness of chronic hepatitis C patients to IFN-alpha therapy.MethodsForty-four individuals who had resolved HCV infection spontaneously and 147 patients who developed chronic hepatitis C were analyzed for functional single nucleotide polymorphisms in the promoter regions of the interferon regulatory factor-1 (IRF-1) and myxovirus resistance protein-1 (MxA) genes at positions -300 and -88, respectively.ResultsWith regard to -300 IRF-1 or -88 MxA genotype distributions or minor allele frequencies, individuals who spontaneously resolved the infection displayed no significant difference compared with those with chronic infections. Among patients with chronic infections, however, the -300AA IRF-1 genotype, associated with a higher IRF-1 transcriptional activity, was absent in patients with chronic HCV genotype 3a infections, with one exception. In contrast to expectations, -300AA IRF-1 individuals with HCV genotype 3a infection were not represented in higher numbers among those with self-limited infections. Regarding IFN-alpha therapy, -300AA IRF-1 chronic hepatitis C genotype 1 patients tend to respond more often than those with the other IRF-1 genotypes.ConclusionOur findings suggest the possibility that the -300AA IRF-1 genotype is associated with outcome in patients with HCV genotype 3 infection. In addition, in HCV genotype-1-infected patients, this genotype appears associated with response to therapy."xsd:string |
http://purl.uniprot.org/citations/16894313 | http://purl.org/dc/terms/identifier | "doi:10.1097/01.meg.0000224478.89545.76"xsd:string |
http://purl.uniprot.org/citations/16894313 | http://purl.uniprot.org/core/author | "Ramadori G."xsd:string |
http://purl.uniprot.org/citations/16894313 | http://purl.uniprot.org/core/author | "Bickeboller H."xsd:string |
http://purl.uniprot.org/citations/16894313 | http://purl.uniprot.org/core/author | "Mihm S."xsd:string |
http://purl.uniprot.org/citations/16894313 | http://purl.uniprot.org/core/author | "Manhardt L.B."xsd:string |
http://purl.uniprot.org/citations/16894313 | http://purl.uniprot.org/core/author | "Maouzi A.B."xsd:string |
http://purl.uniprot.org/citations/16894313 | http://purl.uniprot.org/core/author | "Wietzke-Braun P."xsd:string |
http://purl.uniprot.org/citations/16894313 | http://purl.uniprot.org/core/date | "2006"xsd:gYear |
http://purl.uniprot.org/citations/16894313 | http://purl.uniprot.org/core/name | "Eur J Gastroenterol Hepatol"xsd:string |
http://purl.uniprot.org/citations/16894313 | http://purl.uniprot.org/core/pages | "991-997"xsd:string |
http://purl.uniprot.org/citations/16894313 | http://purl.uniprot.org/core/title | "Interferon regulatory factor-1 promoter polymorphism and the outcome of hepatitis C virus infection."xsd:string |
http://purl.uniprot.org/citations/16894313 | http://purl.uniprot.org/core/volume | "18"xsd:string |
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