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dc.contributor.authorBridge, SHen_US
dc.contributor.authorPagano, Sen_US
dc.contributor.authorJones, Men_US
dc.contributor.authorFoster, GRen_US
dc.contributor.authorNeely, Den_US
dc.contributor.authorVuilleumier, Nen_US
dc.contributor.authorBassendine, MFen_US
dc.date.accessioned2018-05-15T07:37:06Z
dc.date.available2018-01-08en_US
dc.date.issued2018-01en_US
dc.date.submitted2018-03-29T14:34:12.423Z
dc.identifier.urihttp://qmro.qmul.ac.uk/xmlui/handle/123456789/38103
dc.description.abstractBACKGROUND/PURPOSE: One to three per cent of the world's population has hepatitis C virus (HCV) infection, which is not only a major cause of liver disease and cancer but also associated with an increased risk of atherosclerosis, despite an ostensibly favourable lipid profile. Autoantibodies are frequent in HCV infection and emerging evidence shows that autoantibodies could be valuable for cardiovascular disease (CVD) risk stratification. This study investigated a novel independent biomarker of CVD, autoantibodies to apolipoprotein A-1 (anti-apoA-1 IgG) and lipids in patients with chronic HCV before, during and after direct-acting anti-viral (DAA) therapy. METHODS: Eighty-nine blinded serum samples from 27 patients with advanced chronic HCV were assayed for lipids and anti-apoA-1 IgG by ELISA. RESULTS: Pre-treatment HCV viral load correlated with high-density lipoprotein cholesterol (HDL-C, r = 0.417; p = 0.042) and negatively with apolipoprotein (apo)B (r = - 0.497; p = 0.013) and markers of CVD risk, the apoB/apoA-1 ratio (r = - 0.490; p = 0.015) and triglyceride level (TG)/HDL-C ratio (r = - 0.450; p = 0.031). Fourteen (52%) of 27 patients had detectable anti-apoA-1 IgG autoantibodies pre-treatment; only two became undetectable with virological cure. Autoantibody-positive sera had lower apoA-1 (p = 0.012), HDL-C (p = 0.009) and total cholesterol (p = 0.006) levels. CONCLUSIONS: This is the first report of the presence of an emerging biomarker for atherosclerosis, anti-apoA-1 IgG, in some patients with HCV infection. It may be induced by apoA-1 on the surface of HCV lipoviral particles. The autoantibodies inversely correlate with apoA-1 and HDL levels and may render HDL dysfunctional. Whether these hypothesis-generating findings have clinical implications in HCV patients requires further study.en_US
dc.description.sponsorshipSHB received financial support from an Anniversary Research Fellowship from Northumbria University. GRF received speaker and consultancy fees from Abbvie, Gilead, BMS (Bristol Myers Squibb), Janssen, Tekmira, Merck and Alcura.en_US
dc.format.extent17 - 25en_US
dc.languageengen_US
dc.relation.ispartofHepatol Inten_US
dc.rightsThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
dc.subjectApolipoprotein A-1en_US
dc.subjectAtherosclerosisen_US
dc.subjectAutoimmunityen_US
dc.subjectCardiovascular risken_US
dc.subjectHepatitis C virusen_US
dc.subjectAgeden_US
dc.subjectApolipoprotein A-Ien_US
dc.subjectAutoantibodiesen_US
dc.subjectBiomarkersen_US
dc.subjectCholesterol, HDLen_US
dc.subjectCholesterol, LDLen_US
dc.subjectCoronary Artery Diseaseen_US
dc.subjectFemaleen_US
dc.subjectHepacivirusen_US
dc.subjectHepatitis Cen_US
dc.subjectHumansen_US
dc.subjectMaleen_US
dc.subjectMiddle Ageden_US
dc.subjectSensitivity and Specificityen_US
dc.subjectViral Loaden_US
dc.titleAutoantibody to apolipoprotein A-1 in hepatitis C virus infection: a role in atherosclerosis?en_US
dc.typeArticle
dc.rights.holder© The Author(s) 2018
dc.identifier.doi10.1007/s12072-018-9842-5en_US
pubs.author-urlhttps://www.ncbi.nlm.nih.gov/pubmed/29423541en_US
pubs.issue1en_US
pubs.notesNot knownen_US
pubs.organisational-group/Queen Mary University of London
pubs.organisational-group/Queen Mary University of London/Faculty of Medicine & Dentistry
pubs.organisational-group/Queen Mary University of London/Faculty of Medicine & Dentistry/Blizard Institute
pubs.organisational-group/Queen Mary University of London/Faculty of Medicine & Dentistry/Blizard Institute/Immunobiology
pubs.organisational-group/Queen Mary University of London/REF
pubs.organisational-group/Queen Mary University of London/REF/REF - Blizard
pubs.publication-statusPublisheden_US
pubs.volume12en_US
dcterms.dateAccepted2018-01-08en_US


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