Authors
Simon H Bridge, David A Sheridan, Daniel J Felmlee, Mary ME Crossey, Fiona I Fenwick, Clare V Lanyon, Geneviève Dubuc, Nabil G Seidah, Jean Davignon, Howard C Thomas, Simon D Taylor-Robinson, Geoffrey L Toms, R Dermot G Neely, Margaret F Bassendine
Publication date
2015/4/1
Journal
Journal of hepatology
Volume
62
Issue
4
Pages
763-770
Publisher
Elsevier
Description
Background & Aims
Hepatitis C virus (HCV) associates with lipoproteins to form “lipoviral particles” (LVPs) that can facilitate viral entry into hepatocytes. Initial attachment occurs via heparan sulphate proteoglycans and low-density lipoprotein receptor (LDLR); CD81 then mediates a post-attachment event. Proprotein convertase subtilisin kexin type 9 (PCSK9) enhances the degradation of the LDLR and modulates liver CD81 levels. We measured LVP and PCSK9 in patients chronically infected with HCV genotype (G)3. PCSK9 concentrations were also measured in HCV-G1 to indirectly examine the role of LDLR in LVP clearance.
Methods
HCV RNA, LVP (d <1.07 g/ml) and non-LVP (d >1.07 g/ml) fractions, were quantified in patients with HCV-G3 (n = 39) by real time RT-PCR and LVP ratios (LVPr; LVP/(LVP + non-LVP)) were calculated. Insulin resistance (IR) was assessed using the homeostasis model assessment …
Scholar articles
SH Bridge, DA Sheridan, DJ Felmlee, MME Crossey… - Journal of hepatology, 2015