Autoantibody to apolipoprotein A-1 in hepatitis C virus infection: a role in atherosclerosis?

Bridge, Simon, Pagano, Sabrina, Jones, Meleri, Foster, Graham, Neely, Derrmot, Vuilleumier, Nicolas and Bassendine, Margaret (2018) Autoantibody to apolipoprotein A-1 in hepatitis C virus infection: a role in atherosclerosis? In: The International Liver Congress 2018, 11th - 15th April 2018, Paris, France.

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Background and Aims: 1–3% of theworld’s population have 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 (antiapoA-1 IgG) and lipids in patients with chronic HCV before, during and after direct-acting anti-viral (DAA) therapy.

Methods: 89 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, apoB/apoA-1 ratio (r = −0.490; p = 0.015) and triglyceride (TG):HDL ratio (r = −0.450; p = 0.031). There was no significant difference in the serum lipid concentrations at week 0 and 12 of DAA therapy, when all 27 patients had a virologic response (undetectable HCV RNA). 14/27 (52%) patients had detectable antiapoA-1 IgG autoantibodies pre-treatment; only two became undetectable with virologic cure. Autoantibody positive sera had lower apoA-1 (p = 0.012), HDL-C (p = 0.009) and total cholesterol (p = 0.006) levels.

Conclusion: This is the first report of the presence of an emerging biomarker for atherosclerosis, anti-apoA-1 IgG, in some patients with HCV infection. They may be induced by apoA-1 on the surface of HCV lipoviral particles. The autoantibodies inversely correlate with apoA1 and HDL levels and may render HDL dysfunctional. Whether these hypothesis-generating findings have clinical implications in HCV patients requires further study.

Item Type: Conference or Workshop Item (Poster)
Subjects: B900 Others in Subjects allied to Medicine
C700 Molecular Biology, Biophysics and Biochemistry
Department: Faculties > Health and Life Sciences > Applied Sciences
Depositing User: Paul Burns
Date Deposited: 19 Jul 2019 09:33
Last Modified: 10 Oct 2019 16:48

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