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dc.contributor.authorEslam, M
dc.contributor.authorHashem, AM
dc.contributor.authorLeung, R
dc.contributor.authorRomero-Gomez, M
dc.contributor.authorBerg, T
dc.contributor.authorDore, GJ
dc.contributor.authorChan, HLK
dc.contributor.authorIrving, WL
dc.contributor.authorSheridan, David
dc.contributor.authorAbate, ML
dc.contributor.authorAdams, LA
dc.contributor.authorMangia, A
dc.contributor.authorWeltman, M
dc.contributor.authorBugianesi, E
dc.contributor.authorSpengler, U
dc.contributor.authorShaker, O
dc.contributor.authorFischer, J
dc.contributor.authorMollison, L
dc.contributor.authorCheng, W
dc.contributor.authorPowell, E
dc.contributor.authorNattermann, J
dc.contributor.authorRiordan, S
dc.contributor.authorMcLeod, D
dc.contributor.authorArmstrong, NJ
dc.contributor.authorDouglas, MW
dc.contributor.authorLiddle, C
dc.contributor.authorBooth, DR
dc.contributor.authorGeorge, J
dc.contributor.authorAhlenstiel, G
dc.date.accessioned2016-01-26T21:44:50Z
dc.date.available2016-01-26T21:44:50Z
dc.date.issued2015-05
dc.identifier.issn2041-1723
dc.identifier.issn2041-1723
dc.identifier.other6422
dc.identifier.urihttp://hdl.handle.net/10026.1/4237
dc.description.abstract

<jats:title>Abstract</jats:title><jats:p>Tissue fibrosis is a core pathologic process that contributes to mortality in ~45% of the population and is likely to be influenced by the host genetic architecture. Here we demonstrate, using liver disease as a model, that a single-nucleotide polymorphism (<jats:italic>rs12979860)</jats:italic> in the intronic region of interferon-λ4 (IFNL4) is a strong predictor of fibrosis in an aetiology-independent manner. In a cohort of 4,172 patients, including 3,129 with chronic hepatitis C (CHC), 555 with chronic hepatitis B (CHB) and 488 with non-alcoholic fatty liver disease (NAFLD), those with rs12979860CC have greater hepatic inflammation and fibrosis. In CHC, those with rs12979860CC also have greater stage-constant and stage-specific fibrosis progression rates (<jats:italic>P</jats:italic>&lt;0.0001 for all). The impact of rs12979860 genotypes on fibrosis is maximal in young females, especially those with HCV genotype 3. These findings establish rs12979860 genotype as a strong aetiology-independent predictor of tissue inflammation and fibrosis.</jats:p>

dc.format.extent0-0
dc.format.mediumElectronic
dc.languageen
dc.language.isoen
dc.publisherSpringer Science and Business Media LLC
dc.subjectCohort Studies
dc.subjectFemale
dc.subjectGenotype
dc.subjectHepatitis, Chronic
dc.subjectHumans
dc.subjectInterleukins
dc.subjectLiver
dc.subjectLiver Cirrhosis
dc.subjectLogistic Models
dc.subjectNon-alcoholic Fatty Liver Disease
dc.subjectPolymorphism, Single Nucleotide
dc.subjectSex Factors
dc.subjectStatistics, Nonparametric
dc.titleInterferon-λ rs12979860 genotype and liver fibrosis in viral and non-viral chronic liver disease
dc.typejournal-article
dc.typeJournal Article
dc.typeMulticenter Study
dc.typeResearch Support, Non-U.S. Gov't
plymouth.author-urlhttps://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000352633900006&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=11bb513d99f797142bcfeffcc58ea008
plymouth.issue0
plymouth.volume6
plymouth.publication-statusPublished online
plymouth.journalNature Communications
dc.identifier.doi10.1038/ncomms7422
plymouth.organisational-group/Plymouth
plymouth.organisational-group/Plymouth/Faculty of Health
plymouth.organisational-group/Plymouth/Faculty of Health/Peninsula Medical School
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA/UoA01 Clinical Medicine
plymouth.organisational-group/Plymouth/Users by role
plymouth.organisational-group/Plymouth/Users by role/Academics
dc.publisher.placeEngland
dcterms.dateAccepted2015-01-28
dc.identifier.eissn2041-1723
dc.rights.embargoperiodNot known
rioxxterms.versionofrecord10.1038/ncomms7422
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.licenseref.startdate2015-05
rioxxterms.typeJournal Article/Review


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