http://purl.uniprot.org/citations/17489060 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/17489060 | http://www.w3.org/2000/01/rdf-schema#comment | "BackgroundHepatitis C virus infection is a major cause of nonA, nonB hepatitis worldwide. A high prevalence of immunological abnormalities has been shown to occur in patients with chronic hepatitis C virus infection.AimThe aim of this study was to assess the development of sicca syndrome in a cohort of patients infected with a single strain of hepatitis C virus, namely genotype 1b, and correlate this with viral persistence and human leukocyte antigen type of the patients.MethodsNinety-five patients infected with the single strain hepatitis C virus were used in this study, 32 of whom were polymerase chain reaction-negative and 63 polymerase chain reaction-positive. Patient details were reviewed for symptoms consistent with sicca syndrome. Human leukocyte antigen class I (A, B and C) and class II (DRB and DQB1) typing was performed on all patients. Auto-antibodies were also measured.ResultsDQB1*02 was highly significantly associated with viral persistence (P<0.0001). Nineteen of 21 patients with sicca syndrome were hepatitis C virus-polymerase chain reaction-positive demonstrating a strong association with viral persistence and the development of the syndrome. Human leukocyte antigen DQB1*02 was significantly associated with the development of sicca syndrome, P=0.02.ConclusionThe development of autoimmune disease in patients with chronic hepatitis C virus infection depends on the interaction of multiple factors. This study suggests that important factors in this process are viral persistence and human leukocyte antigen type of the patients."xsd:string |
http://purl.uniprot.org/citations/17489060 | http://purl.org/dc/terms/identifier | "doi:10.1097/meg.0b013e328010687d"xsd:string |
http://purl.uniprot.org/citations/17489060 | http://purl.uniprot.org/core/author | "Kelleher D."xsd:string |
http://purl.uniprot.org/citations/17489060 | http://purl.uniprot.org/core/author | "O'Regan M."xsd:string |
http://purl.uniprot.org/citations/17489060 | http://purl.uniprot.org/core/author | "Hagan R."xsd:string |
http://purl.uniprot.org/citations/17489060 | http://purl.uniprot.org/core/author | "Lawlor E."xsd:string |
http://purl.uniprot.org/citations/17489060 | http://purl.uniprot.org/core/author | "McKiernan S.M."xsd:string |
http://purl.uniprot.org/citations/17489060 | http://purl.uniprot.org/core/author | "Smyth C.M."xsd:string |
http://purl.uniprot.org/citations/17489060 | http://purl.uniprot.org/core/author | "Pilkington R."xsd:string |
http://purl.uniprot.org/citations/17489060 | http://purl.uniprot.org/core/date | "2007"xsd:gYear |
http://purl.uniprot.org/citations/17489060 | http://purl.uniprot.org/core/name | "Eur J Gastroenterol Hepatol"xsd:string |
http://purl.uniprot.org/citations/17489060 | http://purl.uniprot.org/core/pages | "493-498"xsd:string |
http://purl.uniprot.org/citations/17489060 | http://purl.uniprot.org/core/title | "Chronic hepatitis C infection and sicca syndrome: a clear association with HLA DQB1*02."xsd:string |
http://purl.uniprot.org/citations/17489060 | http://purl.uniprot.org/core/volume | "19"xsd:string |
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