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dc.contributor.authorBridge, SH
dc.contributor.authorPagano, S
dc.contributor.authorJones, M
dc.contributor.authorFoster, GR
dc.contributor.authorNeely, D
dc.contributor.authorVuilleumier, N
dc.contributor.authorBassendine, MF
dc.date.accessioned2018-05-15T07:37:06Z
dc.date.issued2018-02-08
dc.date.issued2018-01
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.
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 - 25
dc.languageeng
dc.relation.ispartofHepatol Int
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-1
dc.subjectAtherosclerosis
dc.subjectAutoimmunity
dc.subjectCardiovascular risk
dc.subjectHepatitis C virus
dc.titleAutoantibody to apolipoprotein A-1 in hepatitis C virus infection: a role in atherosclerosis?
dc.typeJournal Article
dc.rights.holder© The Author(s) 2018
dc.identifier.doi10.1007/s12072-018-9842-5
pubs.author-urlhttps://www.ncbi.nlm.nih.gov/pubmed/29423541
pubs.issue1
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.publication-statusPublished
pubs.volume12


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