Abstract
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. Eighty-nine blinded serum samples from 27 patients with advanced chronic HCV were assayed for lipids and anti-apoA-1 IgG by ELISA. 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. 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.
Highlights
It is estimated that 1–3% of the world’s population has chronic hepatitis C virus (HCV) infection, which is a major cause of liver disease and liver cancer
Autoantibody-positive sera had lower Apolipoprotein A-1 (apoA-1) (p = 0.012), high-density lipoprotein (HDL)-C (p = 0.009) and total cholesterol (p = 0.006) levels. This is the first report of the presence of an emerging biomarker for atherosclerosis, anti-apoA-1 IgG, in some patients with HCV infection
Blinded serial serum samples (n = 89) from 27 patients with chronic hepatitis C infection undergoing direct-acting anti-viral (DAA) therapy were assayed for viral load, lipids and anti-apoA-1 IgG (AAA1)
Summary
It is estimated that 1–3% of the world’s population has chronic hepatitis C virus (HCV) infection, which is a major cause of liver disease and liver cancer. HCV-infected patients have increased rates of atherosclerosis, which leads to a higher risk of cardiovascular [1] and cerebrovascular morbidity and mortality [2]. Autoantibodies against apolipoprotein A-1 (anti-apoA-1 IgG) have emerged as an independent biomarker for cardiovascular disease and mortality in several populations [6, 7]. These autoantibodies may be mediators of plaque vulnerability [8]. The presence of anti-apoA-1 autoantibodies is a risk biomarker for cardiovascular disease in type 2 diabetes mellitus [10], which is increased in HCV infection [11]
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