Source:http://linkedlifedata.com/resource/pubmed/id/16440356
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2006-2-1
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pubmed:abstractText |
Patients infected with HIV-1 who are heterozygous at HLA class I loci present greater variety of antigenic peptides to CD8+ cytotoxic T lymphocytes, slowing progression to AIDS. A similar broad immune response in chronic hepatitis C (CHC) infection could result in greater hepatic injury. Although specific HLA class II alleles may influence outcome in CHC patients, the role of HLA class I heterogeneity is generally less clearly defined. Our aims were to determine whether HLA class I allelic diversity is associated with disease severity and progression of fibrosis in CHC. The study population consisted of 670 adults with CHC, including 155 with advanced cirrhosis, and 237 non-HCV-infected controls. Serological testing for HLA class I antigens was performed via microlymphocytotoxicity assay. Peptide expression was defined as heterozygous (i.e., a different allele at each locus) or homozygous. Fibrosis staging was determined using METAVIR classification. Heterozygosity at the B locus (fibrosis progression rate [FPR] 0.08 vs. 0.06 units/yr; P = .04) and homozygosity at the A locus (FPR 0.10 vs. 0.08 units/yr; P = .04) predicted a higher median FPR. Age at infection, genotype, and duration of infection were also predictors of FPR. A higher proportion of patients with stage F2-F4 expressed HLA-B18 compared with controls (OR 2.2, 95% CI 1.17-4.23; P = .02). These differences were not observed in patients with advanced cirrhosis. HLA zygosity at 1, 2, or 3 alleles was not associated with fibrosis stage, liver inflammation, or treatment outcome. In conclusion, HLA class I allelic diversity has a minor influence on FPRs and disease severity in CHC.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0270-9139
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pubmed:author |
pubmed-author:BlattLawrence MLM,
pubmed-author:ClareMichaelM,
pubmed-author:ConradAndrewA,
pubmed-author:FengAnneA,
pubmed-author:KoziolJamesJ,
pubmed-author:LebeckLauralynnL,
pubmed-author:McHutchisonJohn GJG,
pubmed-author:NorrisSuzanneS,
pubmed-author:PatelKeyurK,
pubmed-author:PiankoStephenS,
pubmed-author:PortmannBernardB
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pubmed:issnType |
Print
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pubmed:volume |
43
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
241-9
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:16440356-Adult,
pubmed-meshheading:16440356-Disease Progression,
pubmed-meshheading:16440356-Female,
pubmed-meshheading:16440356-Gene Frequency,
pubmed-meshheading:16440356-Genes, MHC Class I,
pubmed-meshheading:16440356-Genetic Variation,
pubmed-meshheading:16440356-Hepatitis C, Chronic,
pubmed-meshheading:16440356-Heterozygote,
pubmed-meshheading:16440356-Humans,
pubmed-meshheading:16440356-Liver,
pubmed-meshheading:16440356-Liver Cirrhosis,
pubmed-meshheading:16440356-Male,
pubmed-meshheading:16440356-Middle Aged,
pubmed-meshheading:16440356-Retrospective Studies
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pubmed:year |
2006
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pubmed:articleTitle |
HLA class I allelic diversity and progression of fibrosis in patients with chronic hepatitis C.
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pubmed:affiliation |
Division of Gastroenterology, Duke Clinical Research Institute, Duke University Medical Center, Durham, NC 27715, USA.
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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