| pubmed-article:19674288 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19674288 | lifeskim:mentions | umls-concept:C0042769 | lld:lifeskim |
| pubmed-article:19674288 | lifeskim:mentions | umls-concept:C0042333 | lld:lifeskim |
| pubmed-article:19674288 | lifeskim:mentions | umls-concept:C1835407 | lld:lifeskim |
| pubmed-article:19674288 | lifeskim:mentions | umls-concept:C1413460 | lld:lifeskim |
| pubmed-article:19674288 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:19674288 | pubmed:dateCreated | 2010-5-7 | lld:pubmed |
| pubmed-article:19674288 | pubmed:abstractText | Claudin-1 is a recently discovered co-receptor for hepatitis C virus (HCV) that is required for late-stage binding of the virus. Because variants in the gene that encodes claudin-1 (CLDN1) could play a role in HCV infection, we conducted a 'whole gene association study' among injection drug users (IDUs) to examine whether CLDN1 genetic variants were associated with the risk of HCV infection or with viral clearance. In a cross sectional study, we examined genotype results for 50 single nucleotide polymorphisms (SNPs) across the CLDN1 gene region, comparing genotypes among participants with chronic HCV (n = 658) to those in IDUs who had cleared HCV (n = 199) or remained HCV-uninfected (n = 68). Analyses were controlled for racial ancestry (African-American or European-American) by stratification and logistic regression modeling. We found that participants who remained uninfected more often carried CLDN1 promoter region SNPs -15312C [odds ratio (OR), 1.72; 95% confidence interval (CI) 1.00-2.94; P = 0.048], -7153A (OR, 2.13; 95% CI, 1.25-3.62; P = 0.006) and -5414C (OR, 1.78; 95% CI, 1.06-3.00; P = 0.03). HCV-uninfected participants less often carried CLDN1 IVS1-2983C (OR, 0.55; 95% CI, 0.31-0.97; P = 0.04), which lies in intron 1. CLDN1 -15312C, -7153A and -5414C formed a haplotype in both the African-American and European-American participants and a haplotype analysis supported the association of CLDN1 -7153A in the HCV-uninfected participants. The analyses of HCV clearance revealed no associations with any SNP. These results indicate that genetic variants in regulatory regions of CLDN1 may alter susceptibility to HCV infection. | lld:pubmed |
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| pubmed-article:19674288 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19674288 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19674288 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:19674288 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19674288 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:19674288 | pubmed:issn | 1365-2893 | lld:pubmed |
| pubmed-article:19674288 | pubmed:author | pubmed-author:BrownMM | lld:pubmed |
| pubmed-article:19674288 | pubmed:author | pubmed-author:ChenSS | lld:pubmed |
| pubmed-article:19674288 | pubmed:author | pubmed-author:RichC RCR | lld:pubmed |
| pubmed-article:19674288 | pubmed:author | pubmed-author:HutchinsonA... | lld:pubmed |
| pubmed-article:19674288 | pubmed:author | pubmed-author:EdlinB RBR | lld:pubmed |
| pubmed-article:19674288 | pubmed:author | pubmed-author:BuschM PMP | lld:pubmed |
| pubmed-article:19674288 | pubmed:author | pubmed-author:O'BrienT RTR | lld:pubmed |
| pubmed-article:19674288 | pubmed:author | pubmed-author:ChanockS JSJ | lld:pubmed |
| pubmed-article:19674288 | pubmed:author | pubmed-author:YeagerMM | lld:pubmed |
| pubmed-article:19674288 | pubmed:author | pubmed-author:XiaoNN | lld:pubmed |
| pubmed-article:19674288 | pubmed:author | pubmed-author:von HahnTT | lld:pubmed |
| pubmed-article:19674288 | pubmed:author | pubmed-author:BekkerVV | lld:pubmed |
| pubmed-article:19674288 | pubmed:author | pubmed-author:DotrangMM | lld:pubmed |
| pubmed-article:19674288 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19674288 | pubmed:volume | 17 | lld:pubmed |
| pubmed-article:19674288 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19674288 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19674288 | pubmed:pagination | 192-200 | lld:pubmed |
| pubmed-article:19674288 | pubmed:dateRevised | 2011-9-29 | lld:pubmed |
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| pubmed-article:19674288 | pubmed:meshHeading | pubmed-meshheading:19674288... | lld:pubmed |
| pubmed-article:19674288 | pubmed:year | 2010 | lld:pubmed |
| pubmed-article:19674288 | pubmed:articleTitle | Genetic variation in CLDN1 and susceptibility to hepatitis C virus infection. | lld:pubmed |
| pubmed-article:19674288 | pubmed:affiliation | Section on Genomic Variation, Pediatric Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. | lld:pubmed |
| pubmed-article:19674288 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19674288 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:19674288 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:19674288 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
