Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
, 35 (1), 87-100

Lipids and HCV


Lipids and HCV

M F Bassendine et al. Semin Immunopathol.


Chronic hepatitis C virus (HCV) infection is associated with an increase in hepatic steatosis and a decrease in serum levels of total cholesterol, low-density lipoprotein cholesterol (LDL) and apolipoprotein B (apoB), the main protein constituent of LDL and very low-density lipoprotein (VLDL). These changes are more marked in HCV genotype 3 infection, and effective treatment results in their reversal. Low lipid levels in HCV infection correlate not only with steatosis and more advanced liver fibrosis but also with non-response to interferon-based therapy. The clinical relevance of disrupted lipid metabolism reflects the fact that lipids play a crucial role in the life cycle of hepatitis C virus. HCV assembly and maturation in hepatocytes depend on microsomal triglyceride transfer protein and apoB in a manner that parallels the formation of VLDL. VLDL production from the liver occurs throughout the day with an estimated 10(18) particles produced every 24 h whilst the estimated hepatitis C virion production rate is 10(12) virions per day. HCV particles in the serum exist as a mixture of complete low-density infectious lipo-viral particles (LVP) and a vast excess of apoB-associated empty nucleocapsid-free sub-viral particles that are complexed with anti-HCV envelope antibodies. Apolipoprotein E (apoE) is also involved in HCV particle morphogenesis and is an essential apolipoprotein for HCV infectivity. ApoE is a critical ligand for the receptor-mediated removal of triglyceride rich lipoprotein (TRL) remnants by the liver. The dynamics of apoB-associated lipoproteins, including HCV-LVP, change post-prandially with an increase in large TRL remnants and very low density HCV-LVP which are rapidly cleared by the liver (at least three HCV receptors are cellular receptors for uptake of TRL remnants). In summary, HCV utilises triglyceride-rich lipoprotein pathways within the liver and the circulation to its advantage.

Similar articles

See all similar articles

Cited by 32 PubMed Central articles

See all "Cited by" articles


    1. Eur J Gastroenterol Hepatol. 2010 Nov;22(11):1303-7 - PubMed
    1. Nat Cell Biol. 2011 Apr;13(4):423-33 - PubMed
    1. Antivir Ther. 2010;15(8):1077-86 - PubMed
    1. Hepatology. 2011 Oct;54(4):1149-56 - PubMed
    1. J Hepatol. 2008 Jul;49(1):9-16 - PubMed

LinkOut - more resources