Apolipoprotein B‐associated cholesterol is a determinant of treatment outcome in patients with chronic hepatitis C virus infection receiving anti‐viral agents interferon‐alpha and ribavirin

<jats:title>Summary</jats:title><jats:p><jats:bold>Background </jats:bold> Hepatitis C virus (HCV) co‐opts very‐low‐density lipoprotein (VLDL) pathways for replication, secretion and entry into hepatocytes and associates with apolipoprotein B (apoB) in plasma. Each VLDL contains apoB‐100 and variable amounts of apolipoproteins E and C, cholesterol and triglycerides.</jats:p><jats:p><jats:bold>Aim </jats:bold> To determine whether baseline lipid levels predicted treatment outcome.</jats:p><jats:p><jats:bold>Methods </jats:bold> Retrospective analysis was performed of 250 chronic hepatitis C (CHC) patients who had received anti‐viral agents interferon‐alpha and ribavirin; 165 had a sustained virological response (SVR). Pre‐ and post‐treatment nonfasting lipid profiles were measured and non‐high‐density lipoprotein (non‐HDL) cholesterol (i.e. apoB‐associated) was calculated. Binary logistic regression analysis assessed factors independently associated with treatment outcome.</jats:p><jats:p><jats:bold>Results </jats:bold> There was an independent association between higher apoB‐associated cholesterol (non‐HDL‐C) and increased odds of SVR (odds ratio 2.09, <jats:italic>P</jats:italic> = 0.042). In multivariate analysis, non‐HDL‐C was significantly lower in HCV genotype 3 (g3) than genotype 1 (<jats:italic>P</jats:italic> = 0.007); this was reversible upon eradication of HCVg3 (pre‐treatment non‐HDL‐C = 2.8 mmol/L, SVR = 3.6 mmol/L, <jats:italic>P</jats:italic> &lt; 0.001).</jats:p><jats:p><jats:bold>Conclusions </jats:bold> Higher apoB‐associated cholesterol is positively associated with treatment outcome in CHC patients receiving anti‐viral therapy, possibly due to competition between apoB‐containing lipoproteins and infectious low‐density HCV lipo‐viral particles for hepatocyte entry via shared lipoprotein receptors.</jats:p>