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Erschienen in: Seminars in Immunopathology 1/2013

01.01.2013 | Review

Lipids and HCV

verfasst von: M. F. Bassendine, D. A. Sheridan, S. H. Bridge, D. J. Felmlee, R. D. G. Neely

Erschienen in: Seminars in Immunopathology | Ausgabe 1/2013

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Abstract

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 1018 particles produced every 24 h whilst the estimated hepatitis C virion production rate is 1012 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.
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Metadaten
Titel
Lipids and HCV
verfasst von
M. F. Bassendine
D. A. Sheridan
S. H. Bridge
D. J. Felmlee
R. D. G. Neely
Publikationsdatum
01.01.2013
Verlag
Springer-Verlag
Erschienen in
Seminars in Immunopathology / Ausgabe 1/2013
Print ISSN: 1863-2297
Elektronische ISSN: 1863-2300
DOI
https://doi.org/10.1007/s00281-012-0356-2

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